The Quantum Lobe Chronicles

Not all hippocampal hemispheres are created equal

2011-11-17T02:46:00.002-05:00

I got a chance to sit down and read Kohl et al.'s recently published Nature Neuroscience paper titled "Hemisphere-specific optogenetic stimulation reveals left-right asymmetry of hippocampal plasticity". This paper contributes to our advancing knowledge of the asymmetrical brain and further elucidates the true complexity of the hippocampus, a sea horse shaped brain structure important for learning and memory.

More specifically, the team found that an area important for encoding and retrieving associated information (CA3) in the left hippocampus produced more long-lasting signal transmission to synapses of an area of the hippocampus important for spatial learning and memory (CA1) compared to CA3 in the right hippocampus of adult mice. Essentially, the left CA3 > right CA3 for triggering plasticity in CA1.

To make their observations Kohl and colleagues used optogenetics in which genetic and optical methods are combined to control specific events in targeted cells of living tissue. In this case, they injected a virus into either the left or right CA3. This particular virus contained a gene which encoded yellow fluorescent protein and led to selective expression of that protein when found in excitatory cells of the appropriately engineered transgenic mice. They then used a laser light to evoke excitatory postsynaptic potentials in the striatum radiatum, an area of the hippocampus that contains fibers connecting CA3 to CA1.

"Brainbow" transgenic mouse hippocampus - Tamily Weissman

The authors explained that the hemispheric asymmetry in plasticity was caused by differential GluN2B gene expression at CA1 synapses targeted by the left and right CA3. They conclude that their result "raises the possibility that the left and right CA3 might be differentially active and hence produce input-specific differences in postsynaptic spines.

However, the question still remains. Why the left and not the right?

(As an aside, I recommend checking out a free iPhone app called 3D Brain. Description: Use your touch screen to rotate and zoom around 29 interactive structures. Discover how each brain region functions, what happens when it is injured, and how it is involved in mental illness. Each detailed structure comes with information on functions, disorders, brain damage, case studies, and links to modern research)

References:

Kohl MM, Shipton OA, Deacon RM, Rawlins JN, Deisseroth K, & Paulsen O (2011). Hemisphere-specific optogenetic stimulation reveals left-right asymmetry of hippocampal plasticity. Nature neuroscience, 14 (11), 1413-5 PMID: 21946328

Can alcoholic parents put their kids at risk for memory problems?

2011-11-13T22:46:00.011-05:00

The alcoholic beverage has existed as early as the Neolithic period (cir. 10,000 BC), its use once mandated by The Lord on High in 1,116 BC China (Patrick, 1952). Oh thou holy ethanol, absorbed by the bloodstream, traveling to the brain, and binding to glutamate and GABA receptors, blessing us with the desired effects of slow reaction time, slurred speech, gregariousness, and the ability to sing and dance like a rockstar. However, too much of the bottle and you can find yourself in some serious trouble, including coma, death (more on alcohol poisoning) and the gradual development of a nasty alcohol addiction (check out Korsakoff's syndrome).

I'm sure we've all experienced the awful sleep and nasty hang over from a forgettable night on the town. My question is can a history of alcoholism cause sleep and cognitive problems not only for the individual, but for the individual's future offspring as well?

An example of fetal alcohol syndrome

Recently, I came across an article by Tarokh and Carskadon (2010) finding that healthy children between ages 9-10 of alcohol abuse/dependent parents had abnormal sleep electroencephalograph activity including reduced delta band and spindle range. Both electrical phenomena are found in non-rapid eye movement (NREM) sleep and are suggested to play 2 important functions; protect sleep from disruption and consolidate declarative memory. The authors believe that the mechanism for the former function may be impaired for these kids. Basically, they'll probably have worse sleep quality compared to their "normal" peers. If this is indeed the case, I don't think that's all that'll be negatively impacted.

In my last post I wrote about how abnormal NREM sleep consisting of reduced spindles and slow wave activity can potentially impair declarative memory (i.e. facts, episodes) through an abnormally functioning thalamus; the sensory relay station of the brain. The kids with alcoholic parents are showing a similar kind of dysfunctional NREM sleep pattern (although the authors only measured spectral power in the spindle range and not spindles directly). Thus, it leads me to believe that they would evidence problems with declarative memory consolidation as well (e.g. remembering what they learned from yesterday's history class).

Are these poor kids being dealt an unfortunate hand consisting of a gimped memory storage system due to their parents' uncontrollable lust for booze? Or is it a matter of genes? Genes/behavior/environment interaction perhaps? A lot more questions than answers it seems.

Of course, this just another crazy hypothesis that I've concocted from thin air that obviously needs empirical support. Quick! To the sleep lab for some more EEG and declarative memory tests! Mom, dad...you can leave that six pack with me.

References:

Tarokh L, & Carskadon MA (2010). Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence. Journal of sleep research, 19 (1 Pt 2), 165-74 PMID: 19735444

Lu W, & Göder R (2011). Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing. Sleep medicine reviews PMID: 21889375

http://www2.potsdam.edu/hansondj/Controversies/1114796842.html

Why Non-rapid Eye Movement (NREM) sleep is important for memory

2011-08-07T02:50:00.013-04:00

So...after 4 months of being MIA I've finally emerged from the deep, dark, and lonely cave of academia to give a brief update on what I've been doing all this time. When I wasn't furiously working on my dissertation related to working memory and aging, I was making final revisions to a theoretical review paper on sleep and memory. I'm happy to announce that after countless hours of lost sleep (irony?) it's finally been accepted for publication! I'll link the article abstract once it's up. For now let's talk about why NREM sleep is important (and why I needed it so badly for the past few months).

During the early years of sleep research, NREM sleep was discovered to play a role in the restoration of physiological functions (Siegal, 2005). However, relatively recently it's been established to play an equally important function, that of sleep-dependent memory consolidation. Some may be asking, "what the bleep is NREM sleep?" Here's the technical answer according to the American Academy of Sleep Medicine. It consists of 3 stages (N1, N2, and N3, very original...) N1 consists of low amp electrical activity measured by electroencephalogram (EEG) where slow eye movements take place. During N2, you're unconscious, but easily awoken. Here, we find seemingly weird blips in electrical brain activity known as k-complexes and sleep spindles. Sleep spindles are super important for memory consolidation, as will be discussed later. N3 (or slow wave sleep) consists of delta waves and peak to peak amps >75uV found in frontal lobes, also very important for sleep-dependent memory consolidation. Now how does all of this electrical activity consolidate memory?

In the early 1970s Ekstrand and colleagues observed that slow wave sleep was positively correlated with the ability to retain a word pair-associate list, while rapid eye movement (REM) sleep was not. They went on to publish their findings in Science. Memorizing these word pairs depend on declarative memory system functioning. Declarative memory is hippocampal-based memory accessible through conscious recollection including facts and events. Ekstrand's findings and many other subsequent studies firmly established that slow wave sleep was indeed important for declarative memory consolidation (check out Diekelmann and Born, 2010 for a comprehensive review).

Another seminal study by Wilson and McNaugton (1994), also published in Science, observed an increased tendency for particular hippocampal place cells that fired during a spatial behavioral task to also fire during subsequent slow wave sleep in rats. This lay the foundation for discovering that memory traces consolidate from short-term to long-term memories by a process involving reactivation of sharp wave-ripples in the hippocampus during sleep.

In a more recent and very cool study, Born and colleagues (2007) had human subject learn card pair locations while smelling different odors simultaneously (the top left card paired with the scent of my feet, for example). When the researchers reintroduced those same smells during the subjects' slow wave sleep (my feet in the poor subject's face), memory for the card pair locations (top left card) tied to those smells (my feet) were enhanced at recall the next day. Also, through fMRI they saw reactivation of the hippocampus during slow wave sleep. In an alternative study, they used transcranial magnetic stimulation to essentially boost slow oscillations during NREM sleep, which not only increased slow wave sleep and sleep spindles, but also enhanced declarative memory consolidation.

From these findings they developed a model postulating that slow waves originating from the neocortex synced both hippocampal sharp waves and thalamocortical sleep spindles, resulting in primed cortical networks for long-term memory storage. The research team was the first to provide empirical support for a causal role of hippocampal memory reactivation for memory enhancement during sleep.

The key point I'm trying to emphasize here is that slow wave sleep and sleep spindle activity are essential for sleep dependent declarative memory consolidation.

The question I pose in my paper (with the invaluable help of Dr. Robert Göder) is what happens to declarative memory consolidation when slow wave sleep and sleep spindle activity, both taking place during NREM sleep, are disrupted? I've definitely experienced the detrimental effects first hand and hope to soon show you, with the latest research, how abnormal NREM sleep can really mess with memory consolidation. For now, I return to my cave to rest my weary head, praying that I don't become an unfortunate case of ABD (all but dissertation) due to lack of sleep.

References:

Siegel, J. (2005). Clues to the functions of mammalian sleep Nature, 437 (7063), 1264-1271 DOI: 10.1038/nature04285

Iber C, Ancoli-Israel S, Chesson A, Quan SF for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events : Rules, Terminology and Technical Specifications, 1st ed. : Wenchester, Minois, American Academy of Sleep Medicine 2007.

Diekelmann, S., & Born, J. (2010). The memory function of sleep Nature Reviews Neuroscience DOI: 10.1038/nrn2762

Fowler MJ, Sullivan MJ, Ekstrand BR. Sleep and memory. Science 1973;79:302-304.

Wilson, M., & McNaughton, B. (1994). Reactivation of hippocampal ensemble memories during sleep Science, 265 (5172), 676-679 DOI: 10.1126/science.8036517

Rasch B, Büchel C, Gais S, & Born J (2007). Odor cues during slow-wave sleep prompt declarative memory consolidation. Science (New York, N.Y.), 315 (5817), 1426-9 PMID: 17347444

Marshall, L., Helgadóttir, H., Mölle, M., & Born, J. (2006). Boosting slow oscillations during sleep potentiates memory Nature, 444 (7119), 610-613 DOI: 10.1038/nature05278

How a stinky chemical offers neuroprotection for a seizing brain

2011-04-17T00:03:00.009-04:00

What did Socrates, Plato, Hercules, and Ajax have in common? Other than greatness, they were also epileptics according to the 17th century French physician, Jean Taxil.

An epileptic seizure consists of abnormal excessive or synchronous neuronal activity in the brain which can lead to convulsions, loss of awareness, full body slump, or even the experience of deja vu. Unprovoked seizures are typically related to epilepsy and other seizure related disorders while unprovoked seizures have multiple contributing factors including, but not limited to traumatic brain injury, kidney failure, sleep deprivation, brain lesions, metabolic disturbances, stroke, and tricyclic antidepressants. Sometimes seizures are just idiopathic (unknown cause).

Is epilepsy really the "sacred disease" Hippocrates had once thought it was? Not really. Serious complications may arise such as difficulty learning, aspiration pneumonia, injury from falls, and even permanent brain damage (I recommend the book The Spirit Catches You and You Fall Down).

A recent study by Bell and colleagues published in the latest Nature Neuroscience investigated whether polyamines, organic compounds having two or more primary amino groups, acted as a neuroprotective factor against subsequent seizures. Past studies have shown that polyamines increase after a seizure, but their regulatory role in epileptic seizures remain a mystery.

The authors exposed Xenopus laevis tadpoles (aka African clawed tadpoles) to pentylenetetrazol (PTZ), a well known convulsant, to see if polyamines would regulate neural excitability following a seizure. After a priming exposure, they again exposed the poor tadpoles to PTZ 4 hours later. What they found was quite remarkable. Compared to a control group (tadpoles that did not receive a priming exposure to PTZ), the seizure onset in the primed group during the second exposure was delayed a whopping 25%. Something was protecting them from having a subsequent seizure, but what was it?

The authors found that a stinky type of polyamine known as prutescine (more like "putrid-scine" ::rimshot::) was involved in decreasing seizure susceptibility. They suggest that when prutescine is released after the first seizure, it converts into GABA, an inhibitory neurotransmitter. The extracellular GABA then activates presynaptic GABA receptors on inhibitory interneurons, temporarily decreasing inhibitory drive and increasing seizure susceptibility (a kindling effect). The inhibitory neurons respond to this activation with a compensatory release of more GABA. When the prutescine and GABA levels return back to normal, the inhibitory frequency stays elevated. When another seizure occurs, the animal is well protected.

The findings of this study shed further light on the development of the seizing brain and bring the field closer to developing preventative measures for both short-term and long-term seizure susceptibility. Prutescine may indeed be the golden ticket to improving resiliency to seizures. Now all we need to figure out is what to do with that horrific stench.

Bell MR, Belarde JA, Johnson HF, & Aizenman CD (2011). A neuroprotective role for polyamines in a Xenopus tadpole model of epilepsy. Nature neuroscience, 14 (4), 505-12 PMID: 21378970

Disorder promotes stereotyping

2011-04-09T12:01:00.007-04:00

It'll be interesting to see how this all plays out. Shame on you Stapel!

Xenophobic exclusion has been ubiquitous throughout history. However, the explanation of such a phenomenon has been little understood. Interesting research conducted by Stapel and Lindenberg published in the latest Science has brought us closer to some answers. They found that people who are in a disordered environment (e.g. unclean subway station) exhibit greater discriminatory behavior (e.g. decision to sit further away from a black person compared to a white person). The authors suggest that when the brain faces disorder there is a natural drive for order. One way to reach order is through stereotyping. It's the brain's way of making sense of the world. Too bad it doesn't work all the time.

Editorial Expression of Concern

The report “Coping with chaos: How disordered contexts promote stereotyping and discrimination” by D. A.Stapel and S. Lindenberg (1) reported the effects of the physical environment on human stereotyping and discriminatory behavior. On 31 October 2011, Tilburg University held a press conference to announce interim findings of its investigation into possible data fraud in the body of work published by Stapel. The official report in Dutch (translated into English using Google software) indicates that the extent of the fraud by Stapel is substantial. Pending further details of the Tilburg Committee's findings, Science is publishing this Editorial Expression of Concern to alert our readers that serious concerns have been raised about the validity of the findings in this Report.

Bruce Alberts, Editor-in-Chief

Stapel DA, & Lindenberg S (2011). Coping with chaos: how disordered contexts promote stereotyping and discrimination. Science (New York, N.Y.), 332 (6026), 251-3 PMID: 21474762

Zollner Illusion

2011-03-17T21:31:00.000-04:00

You are not drunk on St. Patty's Day beer (or maybe you are). Those lines are indeed parallel.

Neural enhancement for baseball players

2011-01-13T11:11:00.001-05:00

I've just encountered an interesting blog post on Psychology Today about the positive effects of nicotine on motor functioning and cognition.

"One of the most disturbing was the power of nicotine: 'scientists at the National Institute on Drug Abuse . . . found [it had] ‘significant positive effects' on fine motor skills, the accuracy of short-term memory, some forms of attention, and working memory, among other basic cognitive skills. The improvements ‘likely represent true performance enhancement' and ‘beneficial cognitive effects.'"

It reminds me of why I drink so much coffee.

Indie Video Game Coverage

2010-11-25T10:58:00.004-05:00

A nice break from internship applications...

Cross-cultural personality change throughout the lifespan: a result of brain development?

2010-10-06T15:43:00.027-04:00

It's not difficult to readily imagine the rebellious angst ridden teenager or the wise old man of very few words. McCrae, et al.’s 1999 research findings seem to have validated these prototypical depictions. They found that across various cultures (Germany, Italy, Portugal, Croatia, and South Korea) there were higher levels of neuroticism in young adults and decreases in extraversion and openness in older adults. Older adults also showed increase rates of agreeableness and conscientiousness. But why? The authors offer up some explanations such as a combination of maturational, cultural, cohort and sampling effects. They also briefly mention genetic and evolutionary influences and this is what I am particularly interested in. We know that genes are influenced by evolutionary processes and that brain development is affected by gene expression. I suggest that brain development provides the perfect explanatory mechanism for such changes in personality traits throughout the life span.

Generally, the authors found an increased level of neuroticism in the 18-21 year old range, a sensitive time wrought with angst and rebellion. This makes sense because frontal lobes, responsible for executive functioning and emotional control, are still in development (NIMH). Neurotics tend to respond poorly to environmental stress, interpret ordinary situations as threatening, and are more impulsive. These personality characteristics map well to frontal lobes that have not been fully developed.

The Big Five Personality Traits

The authors also found that adults 50+ years old evidenced lower extraversion and openness and higher agreeableness and conscientiousness. Studies have shown that extraverts demonstrate increased sensitivity to reward signals and novelty seeking, suggesting that the dopaminergic system is involved (Cohen et al., 2005; Golimbet et. al, 2007). One study found that striatal D2 receptor availability predicted socially desirable responding (Reeves et al., 2007). Additionally, age-related decline in dopamine D2 receptors is evident (Volkow et al, 1996, 2000). Taken together these studies may offer up one piece of the explanatory puzzle as to why extraversion declines in older adults.

Openness to experience has been suggested to map well with the orbitofrontal cortex, an area known for decision-making, reward processing and emotional processing (Sutin et al., 2009 ). An absence of the posterior orbital sulcus (a part of the orbitofrontal cortex) in healthy subjects has been positively associated with openness to experience (Roppongi et al., 2010). Interestingly, older adults evidence tissue loss in the orbitofrontal cortex, perhaps explaining the decrease in openness to experience found later in life (Resnick, Lamar, & Driscoll, 2007).

Orbitofrontal Cortex

In terms of agreeablness, one study found that smaller right orbitofrontal lobe volume was associated with low agreeableness while smaller left orbitofrontal volume was correlated with high agreeableness in patients with frontaltemporal dementia (Rankin et al., 2004). Perhaps in normal aging the left orbitofrontal cortex, in particular, gradually loses tissue over time.

Regarding conscientiousness, Jackson, Belota, and Head (2009) discovered that those who were rated as higher on this personality trait showed larger regional volumes in prefrontal and mediotemporal regions and less decline with advanced aging.

The influence of brain development on cross-cultural personality changes in the context of aging, particularly the orbitofrontal cortex, is well worth considering. However, one should not forget about all the other important pieces of the puzzle (i.e. maturational, cultural, cohort and sampling effects). Needless to say, further research needs to be done in order to shed light on this intriguing link between personality and the aging brain.

References:

McCrae RR, Costa PT Jr, Pedroso de Lima M, Simões A, Ostendorf F, Angleitner A, Marusić I, Bratko D, Caprara GV, Barbaranelli C, Chae JH, & Piedmont RL (1999). Age differences in personality across the adult life span: parallels in five cultures. Developmental psychology, 35 (2), 466-77 PMID: 10082017

Cohen MX, Young J, Baek JM, Kessler C, & Ranganath C (2005). Individual differences in extraversion and dopamine genetics predict neural reward responses. Brain research. Cognitive brain research, 25 (3), 851-61 PMID: 16289773

Golimbet, V., Alfimova, M., Gritsenko, I., & Ebstein, R. (2007). Relationship between dopamine system genes and extraversion and novelty seeking Neuroscience and Behavioral Physiology, 37 (6), 601-606 DOI: 10.1007/s11055-007-0058-8

Resnick SM, Lamar M, & Driscoll I (2007). Vulnerability of the orbitofrontal cortex to age-associated structural and functional brain changes. Annals of the New York Academy of Sciences, 1121, 562-75 PMID: 17846159

Reeves SJ, Mehta MA, Montgomery AJ, Amiras D, Egerton A, Howard RJ, & Grasby PM (2007). Striatal dopamine (D2) receptor availability predicts socially desirable responding. NeuroImage, 34 (4), 1782-9 PMID: 17188897

Volkow ND, Wang GJ, Fowler JS, Logan J, Gatley SJ, MacGregor RR, Schlyer DJ, Hitzemann R, & Wolf AP (1996). Measuring age-related changes in dopamine D2 receptors with 11C-raclopride and 18F-N-methylspiroperidol. Psychiatry research, 67 (1), 11-6 PMID: 8797238

Sutin AR, Beason-Held LL, Resnick SM, & Costa PT (2009). Sex differences in resting-state neural correlates of openness to experience among older adults. Cerebral cortex (New York, N.Y. : 1991), 19 (12), 2797-802 PMID: 19366871

Roppongi T, Nakamura M, Asami T, Hayano F, Otsuka T, Uehara K, Fujiwara A, Saeki T, Hayasaka S, Yoshida T, Shimizu R, Inoue T, & Hirayasu Y (2010). Posterior orbitofrontal sulcogyral pattern associated with orbitofrontal cortex volume reduction and anxiety trait in panic disorder. Psychiatry and clinical neurosciences, 64 (3), 318-26 PMID: 20602731

Rankin KP, Rosen HJ, Kramer JH, Schauer GF, Weiner MW, Schuff N, & Miller BL (2004). Right and left medial orbitofrontal volumes show an opposite relationship to agreeableness in FTD. Dementia and geriatric cognitive disorders, 17 (4), 328-32 PMID: 15178947

Jackson J, Balota DA, & Head D (2009). Exploring the relationship between personality and regional brain volume in healthy aging. Neurobiology of aging PMID: 20036035

http://www.nimh.nih.gov/health/publications/teenage-brain-a-work-in-progress-fact-sheet/index.shtml

An artist's interpretation of evolution

2010-09-17T12:52:00.004-04:00

Although somewhat of an unscientific account of the history of evolution, this is by far one of the most amazing stop motion films I have ever seen. Titled "BIG BANG BIG BOOM", the artist, BLU, utilized both paint and physical objects (lots of buildings) to recreate his own interpretation of the evolutionary process and what's in store for the future of Earth. Truly a brilliant work of epic proportions; it left me utterly speechless.

BIG BANG BIG BOOM - the new wall-painted animation by BLU from blu on Vimeo.

direction and animation by BLU
production and distribution by ARTSH.it
sountrack by ANDREA MARTIGNONI

The neuroscience of creativity and insight

2010-09-10T03:58:00.011-04:00

Have you ever wondered what was going on in that noggin of yours when on that rare occasion you had an "aha!" moment or found yourself in a creative flow state, where even your screaming girlfriend couldn't snap you out of? Well Dietrich and Kanso over at the American University of Beirut seem to have mapped out the phenomena for us nicely. However, it's not quite as simple as you think.

In their review paper published in this month's Psychological Bulletin, they cover three broad categories related to insight and creativity. They are divergent thinking, artistic creativity, and insight. All studies reviewed used either electroencephalography, event-related potential, or neuroimaging.

The first category they looked at was divergent thinking, the thought process or method used to generate creative ideas by exploring many possible solutions. An example would be furiously brainstorming something interesting to write about on this darn blog. They found that numerous studies using the divergent thinking paradigm had one thing in common, that subjects exhibited some kind of diffuse prefrontal activation. Oddly enough, there was evidence for both increases and decreases in prefrontal activation depending on the study. They suggest that maybe different types of creativity were being tapped into.

Courtesy of Park Lab

Interestingly, people with schizophrenia show reduced prefrontal activation when performing divergent thinking tasks (Takeshi, 2010).

The next category the team covered was artistic creativity. In a particular series of studies, subjects were asked to mentally compose music, visualize abstract concepts, look at paintings, and imagine previously shown drawings; all under EEG monitoring. Activation of motor and temporalparietal regions were evident.

intense looking motor homunculus

The last category discussed was insight. Reviewing the literature they found that the anterior cingulate cortex, involved in early learning and problem solving, was activated by insight problems and that the superior temporal gyrus, involved in the perception of facial expressions, was activated only when successful solutions to those insight problems were found. What is the sound of one hand clapping?!

The take home message Dietrich and Kanso emphasize is that no single brain area, nor a particular hemisphere for that matter, is involved in creativity or insight (contrary to popular belief). The next time your hipster artist friends tell you they're more "right brain" than anything else you can politely correct them by explaining...

I highly recommend you check out the article as there is a lot I did not cover.

References:

Dietrich A, & Kanso R (2010). A review of EEG, ERP, and neuroimaging studies of creativity and insight. Psychological bulletin, 136 (5), 822-48 PMID: 20804237

Takeshi K, Nemoto T, Fumoto M, Arita H, & Mizuno M (2010). Reduced prefrontal cortex activation during divergent thinking in schizophrenia: A multi-channel NIRS study. Progress in neuro-psychopharmacology & biological psychiatry PMID: 20673784

Is recognition without awareness possible?

2010-09-07T01:39:00.006-04:00

It seems common knowledge in the world of neuroscience that episodic memories are formed through conscious awareness. However, a couple of years ago Voss and Paller found that this may not necessarily be the case. They had subjects perform a forced choice recognition task using kaleidoscope images (for novelty's sake). Interestingly, accuracy was highest when subjects reported guessing, thus indicating little awareness that the studied images had been seen before. "This indicates that episodic memory processing was unhelpful, and suggests that subjects responded instead based on pure visual fluency."

In a second study, the team discovered that subjects performed better on tests of episodic memory when they paid divided attention rather than full attention, further validating their findings. In their 2009 paper they concluded by stating that "our findings add weight to the proposal that nonhuman animals utilize visual fluency without episodic memory when performing tasks intended to probe episodic memory."

However, contrary results have recently been published in this month's Learning & Memory. In a replication study Jeneson, Kirwan, and Squire, found that recognition was better when subjects paid full attention to the visual stimuli compared to paying partial attention. In addition, recognition was better when subjects reported some level of confidence as compared to a guess.

Vass and Paller responded to the disconfirming study by running a further study of their own. To resolve the apparent discrepancy they added a simple manipulation to encourage either guessing or confident responding. They found that encouraging guessing increased prevalence and accuracy of guesses relative to the confident responding condition. The authors suggest that both the prevalence and accuracy of guessing can be influenced by whether subjects adopt guessing-friendly strategies. So the lesson here is...guess away!

References:

Voss JL, & Paller KA (2009). Recognition without awareness in humans and its implications for animal models of episodic memory. Communicative & integrative biology, 2 (3), 203-4 PMID: 19641728

Jeneson A, Kirwan CB, & Squire LR (2010). Recognition without awareness: An elusive phenomenon. Learning & memory (Cold Spring Harbor, N.Y.), 17 (9), 454-9 PMID: 20810620

Voss JL, & Paller KA (2010). What makes recognition without awareness appear to be elusive? Strategic factors that influence the accuracy of guesses. Learning & memory (Cold Spring Harbor, N.Y.), 17 (9), 460-8 PMID: 20810621

A new cure for Alzheimers?

2010-07-24T13:33:00.002-04:00

Can sirtuin help prevent the devastating neurodegenerative disease that affects the lives of millions? NYT health section covers the exciting research taking place regarding this special protein.

Theory of everything

2010-06-09T20:50:00.001-04:00

Garrett Lisi, the American-born theoretical physicist, talks about his theory of everything and why living in a van can be cool. Cowabunga!

Aggression spectrum disorders: The distinction between Borderline Personality Disorder and Psychopathy

2010-04-23T09:55:00.009-04:00

I recently read a fascinating book chapter written by William Arsenio titled Happy Victimization: Emotion Dysregulation in The Context of Instrumental, Proactive Aggression. Early in the chapter, the author discussed how according to a study, 4-year-old children tended to predict that a bully would feel happy after pushing around some poor chump on the playground, aka happy victimization (Arsenio & Kramer, 1992). However, at age 6, children who were probed further not only predicted that the bully would feel happy after bullying, but would feel a sense of remorse as well (4-year-olds stuck to their guns). Is this the beginning stages of moral development?

Arsenio went on to describe the possible link between emotion dysregulation and this notion of happy victimization. The victimizer initially feels positive, but then recognizes the victim's negative feelings. This then elicits an involuntary positive or negative affective response depending on a whole host of factors including temperament, empathy, and parental attachment. For most of us, emotional maturity takes its natural course and empathic development occurs. However, those afflicted with borderline personality disorder and psychopathy seem to either steer off the beaten path or miss the bus completely.

Before we speak further about these two truly disturbing personality disorders, an important distinction should be made between two subtypes of aggression mentioned in the reading. 1) Reactive aggression = "hot headed" impulsive angry reaction (ex. I'll punch you in the face because you really pissed me off). 2) Proactive aggression = "cold blooded" aggression used instrumentally to reach some desirable end (ex. I'll punch you in the face because I want your lunch money).

As I read on, I couldn't help but associate the two very different subtypes of aggression with the aforementioned personality disorders. Were adults who displayed frequent and high levels of reactive aggression more prone to being identified as borderline? Similarly, were those displaying frequent and high levels of proactive aggression more prone to being identified as psychopathic? It seemed to fit all too well to be disregarded, but of course that's not all to the story. To clarify where I'm going with this, characterizations of the personality disorders and some solid evidence are in order.

Borderline personality disorder
1. Prolonged disturbance of personality function in a person characterized by depth and variability of moods.The disorder typically involves unusual levels of instability in mood; black and white thinking, or splitting; chaotic and unstable interpersonal relationships, self-image, identity, and behavior; as well as a disturbance in the individual's sense of self.
2. over-active amygdala (i.e. overly responsive to emotion-related stimuli) (Donegan et al., 2003)
3. insecure attachment (i.e. history of verbally/physically abusive parent) (Aaronson et al., 2006)
4. ability to empathize (Fertuck et al., 2009) = intact mirror neuron system?

Psychopathy
1. An abnormal lack of empathy combined with strongly amoral conduct, masked by an ability to appear outwardly normal. They can use charisma, manipulation, and intimidation to control others and to satisfy their own need.
2. under-active amygdala (i.e. unresponsive to emotion-related stimuli) (Blair, 2008)
3. insecure attachment (i.e. history of verbally/physically abusive parent) (Saltaris, 2002)
4. inability to empathize = dysfunctional mirror neuron system? (Fekteau et al., 2008)

My speculative model in sum:

Borderline personality disorder = insecure attachment + overactive amygdala response + functional mirror neuron system => high reactive/impulsive aggression

Psychopathy = insecure attachment + underactive amygdala + dysfunctional mirror neuron system => high proactive/unemotional + reactive/impulsive aggression

Psychopaths = happy victimizers into adulthood?

References:

Aaronson CJ, Bender DS, Skodol AE, & Gunderson JG (2006). Comparison of attachment styles in borderline personality disorder and obsessive-compulsive personality disorder. The Psychiatric quarterly, 77 (1), 69-80 PMID: 16397756

Arsenio, W. F. (2006). Happy Victimization: Emotion Dysregulation in The Context of Instrumental, Proactive Aggression. Snyder, Douglas K. (Ed); Simpson, Jeffry (Ed); Hughes, Jan N. (Ed). (2006). Emotion regulation in couples and families: Pathways to dysfunction and health. (pp. 101-121). Washington, DC, US: American Psychological Association

Blair, R. (2008). Review. The amygdala and ventromedial prefrontal cortex: functional contributions and dysfunction in psychopathy Philosophical Transactions of the Royal Society B: Biological Sciences, 363 (1503), 2557-2565 DOI: 10.1098/rstb.2008.0027

FECTEAU, S., PASCUALLEONE, A., & THEORET, H. (2008). Psychopathy and the mirror neuron system: Preliminary findings from a non-psychiatric sample Psychiatry Research, 160 (2), 137-144 DOI: 10.1016/j.psychres.2007.08.022

Fertuck EA, Jekal A, Song I, Wyman B, Morris MC, Wilson ST, Brodsky BS, & Stanley B (2009). Enhanced 'Reading the Mind in the Eyes' in borderline personality disorder compared to healthy controls. Psychological medicine, 39 (12), 1979-88 PMID: 19460187

Saltaris, C. (2002). Psychopathy in juvenile offenders Can temperament and attachment be considered as robust developmental precursors? Clinical Psychology Review, 22 (5), 729-752 DOI: 10.1016/S0272-7358(01)00122-2

The difference between softcore and hardcore insomnia

2010-04-03T04:20:00.024-04:00

Self-proclaimed insomniacs should be asking themselves right now if they've got either a "softcore" or a "hardcore" sleep problem on their hands. What's the difference between softcore and hardcore insomnia and why is it important you ask? First, let's define the terms.

Softcore insomnia = complaint of insomnia with normal sleep duration greater than or equal to 6 hours of sleep
Hardcore insomnia = complaint of insomnia with less than or equal to 6 hours of sleep

Fernandez-Mendoza and colleagues from Penn State University College of Medicine grouped 678 participants from the general population using the aforementioned criteria (although without the sophisticated categorical nomenclature) to see what between-group differences in neuropsychological performance they would find. They controlled for age, race, gender, education, body mass index, and physical and mental health. The comprehensive neuropsychological battery included tests of processing speed, attention, visual memory, and verbal fluency.

The research team found no difference in performance between softcore insomniacs and controls. However, the hardcore insomniacs did worse on all tests compared to the controls and, get this, controls with less than 6 hours of sleep. Here it seems to be the case that it's only a problem if you make it one. "It's all about perception" as my former professor use to say. Can it be stress, anxiety, or depression combined with the lack of sleep that's leading to poorer performance? Further studies need to be done to tease this all apart.

The most significant finding was that hardcore insomniacs did the worst on tasks that required executive control of attention (set-switching).

If you're truly a hardcore insomniac, do yourself a favor and stay away from multi-tasking. For the rest of you softcore insomniacs, suck it up! At least you don't have real-life cognitive deficits.

References:

ulio Fernandez-Mendoza, MSc1,2,3; Susan Calhoun, PhD1; Edward O. Bixler, PhD1; Slobodanka Pejovic, MD1; Maria Karataraki, PsyD1; Duanping Liao, PhD4; Antonio Vela-Bueno, MD2; Maria J. Ramos-Platon, PhD3; Katherine A. Sauder, BA1; Alexandros N. Vgontzas, M (2010). Insomnia with Objective Short Sleep Duration is Associated with Deficits in Neuropsychological Performance: A General Population Study SLEEP, 33 (4), 459-465

How forming new memories help retain older ones

2010-03-30T03:49:00.024-04:00

Try to remember this visual paired associate (AB):

Now recall visual paired associate AB:

Next, try to remember this new visual paired associate (AC):

Now recall visual paired associate AC:

Can you still remember the first visual paired associate AB? (probably, it wasn't that hard)

What if I were to pay you ten cents to remember? How about if I increased it to a hundred bucks? Would your memory performance increase? Stay the same? Most of your would probably infer the former. More money = more motivation to memorize.

That's what Kuhl and colleagues found in their study published in the latest issue of Nature Neuroscience. However, the study didn't just stop there. That's just the tip of the iceberg!

They had all participants complete a task similar to the one just demonstrated, but used more novel pairings such as a watch and a pipe (yawn). Trials began either with a high or a low reward tagged to an AB pair and a high, low, or no reward tagged to an AC pair (interference). There were 8 encoding and immediate test rounds and 1 critical post-test round conducted outside of the scanner. Here participants were asked to recall AB pairs only. As expected, retroactive interference negatively affected memory retrieval of AB pairs.

Using fMRI, the authors found that left hippocampal activation during the learning of a latter visual paired associate predicted how well the first paired associate would be remembered. Basically, if your left memory cortex didn't light up while encoding new information then the relatively older information was most likely forgotten. More specifically, for those of you who couldn't remember the first pair (horse and no-name comic book) it's highly probable that your left posterior hippocampus and parahippocampal cortex weren't activated during the learning of the latter pair (horse and Sarah Jessica Parker).

Reprinted by permission from Macmillan Publishers Ltd: Nature Neuroscience, advance online publication, 28 February 2010 (doi: 10.1038/sj.nn.2498)

Furthermore, the researchers found that when successful recall for AB pairs were achieved, reward centers in the brain (fronstriatal regions) also lit up on fMRI scan.

So how can all of this be explained? According to the authors, hippocampal reactivation is protecting the stored episodic memories from being forgotten in the face of interfering information. The authors chalk it up to pattern completion which "allows previously encoded memories to be reinstated from a partial input, thereby allowing past episodes to be reactivated, interleaved with current experience, and consolidated over time". The horse not only serves as a retrieval cue for the memory of Sarah Jessica Parker, but the no-name comic book as well.

Additionally, the findings underscore the importance of past reward-associated (motivated) learning and its incorporation into new learning experiences.

(Santiago Ramón y Cajal's drawing of the hippocampus)

This study leads me to wonder what key factors contribute to individual differences in memory encoding after performing an interference task. Is it just hippocampal functioning and level of motivation that sets each and every one of us apart? What about working memory capacity (prefrontal and parietal areas)? Intelligence? Age? Level of alertness? Amount of sleep prior to and/or after learning? All the above? Anyway, it's time to end this pointless musing. Back to more important matters like tending to Ninja Garden Issue 1.

References:

Kuhl, B., Shah, A., DuBrow, S., & Wagner, A. (2010). Resistance to forgetting associated with hippocampus-mediated reactivation during new learning Nature Neuroscience, 13 (4), 501-506 DOI: 10.1038/nn.2498

Parkinsonian emotion recognition impairment better accounted for by sleep deprivation

2010-03-18T14:26:00.186-04:00

The New York Times recently covered a paper by Grey and Tickle-Degnen, published in the journal Neuropsychology, finding that people with Parkinson's Disease (PD) are not able to recognize facial and vocal emotions very well. The article states that it's not clear why this seems to be the case.

I briefly reviewed the original meta-analytic paper (the pdf can be found here) and saw that the research team accounted for 1) the emotion recognition tasks used, 2) the medication the participants were on, and 3) the existence of depression as possible moderatoring variables for the impairment in emotion recognition.

They suggest that "the likely cause of this deficit is pathology in neural circuits involved in emotion recognition, particularly within basal ganglia structures including the ventral striatum and STN." This tentative speculation is just fine and dandy, but it doesn't really provide an explanation for why people with PD have this particular deficit in the first place.

They rule out comorbid depression and visualspatial impairment, but go on to postulate that Lewy bodies disease, an abnormal amount of protein found inside the nerve cells of many PD patients, may be affecting their visual cortex, therefore affecting their emotion recognition abilities. Too bad there's no shred of evidence found in the research literature to support this hypothesis (they make sure to note this).

What I found surprising what that they made no mention of sleep disturbances' possible moderating role in explaining their findings. Drawing from my previous entry on sleep deprivation's deleterious effects on emotion recognition, maybe it's the fact that people suffering from PD commonly have concomitant sleep problems, therefore leading to emotion recognition impairment.

Numerous studies have shown that as many as 42% of PD individuals have some kind of sleep disorder (almost four times as many people compared to people without PD). Other studies have found that PD significantly affects rapid eye movement (REM) sleep behavior leading to a variety of cognitive impairments and sleep disturbances (Massicotte-Marquez et al., 2009, Norlinah et al., 2009, Seugnet et al., 2009,). We now also know that REM sleep is crucial in the processing of emotional memory (Nishida, 2008). And like I said before, sleep deprivation takes a heavy toll on emotion recognition functioning (van der Helm, Gujar, & Walker, 2010). Sleep seems to account for much of our emotional life!

In light of the aforementioned studies, it makes the most sense that sleep deprivation from sleep disturbances would be the more likely pathway to emotional recognition impairment in people with PD; not working memory dysfunction as the authors suggest (although it could most definitely exacerbate matters). There may be many potential sources for interpersonal difficulties in PD individuals who are unable to read emotions accurately. Perhaps future sleep treatment can help prevent such difficulties from ever occurring. Just a thought...

References:

Gray HM, & Tickle-Degnen L (2010). A meta-analysis of performance on emotion recognition tasks in Parkinson's disease. Neuropsychology, 24 (2), 176-91 PMID: 20230112

Massicotte-Marquez J, Décary A, Gagnon JF, Vendette M, Mathieu A, Postuma RB, Carrier J, & Montplaisir J (2008). Executive dysfunction and memory impairment in idiopathic REM sleep behavior disorder. Neurology, 70 (15), 1250-7 PMID: 18216303

Seugnet L, Galvin JE, Suzuki Y, Gottschalk L, & Shaw PJ (2009). Persistent short-term memory defects following sleep deprivation in a drosophila model of Parkinson disease. Sleep, 32 (8), 984-92 PMID: 19725249

Norlinah, M., Afidah, K., Noradina, A., Shamsul, A., Hamidon, B., Sahathevan, R., & Raymond, A. (2009). Sleep disturbances in Malaysian patients with Parkinson's disease using polysomnography and PDSS Parkinsonism & Related Disorders, 15 (9), 670-674 DOI: 10.1016/j.parkreldis.2009.02.012

Jon Kabat-Zinn's Toward a Mindful Society

2010-03-18T01:01:00.003-04:00

I recently found a great interview with creator of the mindfulness-based stress reduction program, Jon Kabat-Zinn, discussing the philosophy, goals, and promise of the mindfulness movement. I highly suggest the read found here.

Apparently they've made a Facebook page promoting his candidacy for Noble Prize in Medicine.

Let me know what you think about the article and whether or not he has a fighting chance. MBSR ftw!

Earworms, lyrics, and tunes in the brain

2010-03-16T01:25:00.018-04:00

Last time I left off quoting Lady GaGa's masterwork Poker Face. I continue to rag on it because I can't seem to escape it's repetitive and forced impingement on my vulnerable eardrums. Unfortunately, the city doesn't afford much auditory privacy and some people in the subway are really determined to lose their hearing before old age. Whatever happened to iPod etiquette?

According to Oliver Sack's book Musicophilia I've got a bad case of the earworm. This is when a piece of music repeats compulsively in one's mind. But if I hate the song so much why is my brain constantly replaying it over and over again? Sacks similarly asks:

What is happening psychologically and neurologically, when a tune or a jingle takes possession of one like this? What are the characteristics that make a tune or a song 'dangerous or 'infectious' in this way? Is it some oddity of sound, of timbre or rhythm or melody? Is it repetition? Or is it arousal of special emotional resonances or associations?

Sacks is onto something here when he makes mention of rhythm and repetition. "Poker Face" has an absurd amount of repetition. The word "mum" is repeated 40 times in the song. The phrase "can't read my" is spoken 30 times. (A link on how to get rid of earworm, wish I had found it sooner)

In any case, have you ever wondered how the brain actually processes lyrics and tunes? There's a hot debate as to whether they are represented as separate components or integrated throughout...but since New Scientist seems to have already covered the paper (doh! I just found out a second ago)...I leave you with the main findings of Sammler et. al's paper published in the latest issue of The Journal of Neuroscience. I also leave you with a gift...in hopes to infect you with an earworm of your own! Misery loves company.

...the left mid-STS showed an interaction of the adaptation effects for lyrics and tunes, suggesting an integrated processing of the two components at prelexical, phonemic processing levels. The degree of integration decayed toward more anterior regions of the left STS, where the lack of such an interaction and the stronger adaptation for lyrics than for tunes was suggestive of an independent processing of lyrics, perhaps resulting from the processing of meaning. Finally, evidence for an integrated representation of lyrics and tunes was found in the left dorsal precentral gyrus (PrCG), possibly relating to the build-up of a vocal code for singing in which musical and linguistic features of song are fused. Overall, these results demonstrate that lyrics and tunes are processed at varying degrees of integration (and separation) through the consecutive processing levels allocated along the posterior–anterior axis of the left STS and the left PrCG.

Sacks, O. (2007). Musicophilia: Tales of music and the brain. New York, NY: Alfred A. Knopf

Sammler, D., Baird, A., Valabregue, R., Clement, S., Dupont, S., Belin, P., & Samson, S. (2010). The Relationship of Lyrics and Tunes in the Processing of Unfamiliar Songs: A Functional Magnetic Resonance Adaptation Study Journal of Neuroscience, 30 (10), 3572-3578 DOI: 10.1523/JNEUROSCI.2751-09.2010

2010 Research Blogging Awards

2010-03-13T19:02:00.001-05:00

Hey guys. Just wanted to remind you that the deadline for votes is tomorrow so click on that icon to the left and VOTE! However, you need to register with researchblogging.org first. So if you contribute to a pretty kick ass science blog using peer-reviewed sources I highly suggest doing so.

By the by, my blog has been nominated in two categories, Best Psychology Blog and Best Neuroscience Blog (thanks to those who nominated the "QLC"). I've got a lot of awesome competition so make sure to check out their sites. Your votes would be greatly appreciated!

Sleep deprivation impairs emotion recognition

2010-03-09T01:10:00.082-05:00

The ability to read emotions is an important part of the human experience; the only way to successfully navigate through complex social environments. It comes in handy especially if you don the title of psychotherapist or professional poker player. Without it, you become socially inept. You enter the world of the autistic individual.

Thanks to Charles Darwin we now know that it’s not just the eyes that are “the windows to the soul”. He first wrote about the subject of facial expressions in his 1898 book titled The Expression of the Emotions in Man and Animals (the link includes the work in its entirety). In it he described the emotions conveyed in the face as being both universal and “species-specific”.

Ekman and Friesen (1969) expounded on Darwin's theory, hypothesizing that universal facial expressions were to be found in the relationship between distinctive patterns of the facial muscles and particular emotions. In 1971 they traveled to Papua New Guinea to test the Fore tribe, a people who had minimal contact with outsiders. The researchers found that the Fore were able to accurately identify the expressions of emotion in photographs of people from cultures with which they were not yet familiar (here's a link to a fascinating NPR Ekman podcast).

An interesting, yet off-topic note: Apparently a Fore subgroup found in southern New Guinea regularly practiced cannibalism by dismembering and eating victims of the prion disease kuru (aka laughing sickness due to the outbursts of laughter during the second phase). Shirley Lindenbaum, a kuru researcher, reported that kuru victims were highly valued as a source of food because the layers of fat resembled pork...yum (Lindenbaum, 1979). Women would often feed brain and various parts of organs to their young and the elderly. Unfortunately, this was yet another mode of kuru transmission. The southern Fore knew better than to eat diseased corpses, but thought that kuru was more a mental affliction than a physical one.

van der Helm and colleagues over at the University of California decided to take a unique look at emotional recognition in the context of sleep. In their recently published SLEEP paper, they asked whether emotional processing would become significantly impaired in sleep deprived individuals.

The authors randomly assigned 37 young adults to either a sleep control or total sleep deprivation group. All participants abstained from caffeine and alcohol three days prior to and three days during the study (sucks to be them). Both groups were asked to perform an emotional facial recognition task at 16:00 for two consecutive days.

The task involved evaluating sad, angry, and happy faces from the Ekman Pictures of facial affect set. The participants were presented with 10 emotionally morphed pictures of the same person and asked to determine which emotion each facial expression was conveying. The control group got to sleep at home like normal people while the not so fortunate sleep-deprivees were kept awake in the sleep lab (at least they had internet!).

(similar morphing method used in the study)

The team found that a single night of sleep deprivation significantly disrupted the ability to identify emotionally salient facial expressions in others. Deficits were most dramatic for emotions eliciting high autonomic arousal (i.e. happy and angry). Interestingly enough, they found that women in particular were more significantly influenced by sleep deprivation on emotion recognition (I suppose evolutionarily it seems to make sense).

They suggest that sleep loss impairs discrete affective neural systems involving the amygdala (fear center of the brain), basal ganglia (lesions here impair anger recognition), the orbitofrontal cortex, and anterior cingulate cortex (activation here is correlated with happy emotions).

(Added the orbitofrontal and anterior cingulate cortex (ACC))

Some study limitations the authors humbly listed include not measuring chronotype (alertness and preference for activity early or late in the day) and motivation/interest level, and not verifying compliance of sleep time and duration (such as using actigraph measurements).

So for all the sleep deprived psychotherapists and the poker players who decide to spend all night at the table, I hope this entry helps you to reconsider such unwise habits. In the words of the um...brilliant Lady GaGa:

Mum mum mum mah
Mum mum mum mah

Can't read my,
Can't read my
No he can't read my poker face

(Decided to randomly plug in these terrible lyrics to show how stupid they are...god, I really need to get this horrid song out of my head...maybe it's time for me to hit the sack)

(...or maybe not)

van der Helm E; Gujar N; Walker MP (2010). Sleep Deprivation Impairs the Accurate Recognition of Human Emotions SLEEP, 33 (3), 335-342

Ekman P, & Friesen WV (1971). Constants across cultures in the face and emotion. Journal of personality and social psychology, 17 (2), 124-9 PMID: 5542557

Steadman, L. (1980). : Kuru Sorcery: Disease and Danger in the New Guinea Highlands . Shirley Lindenbaum. American Anthropologist, 82 (3), 692-694 DOI: 10.1525/aa.1980.82.3.02a01130

How looking away prevents pedestrian collisions

2010-02-28T16:42:00.514-05:00

One day a friend and I were briskly strolling along a mall corridor, engaged in conversation, until something quite hilarious happened. A burly gentleman was quickly approaching my friend's direct line of trajectory. She and this man had to make either one of two choices; move to the left or to the right to avoid a disastrous collision. Simple, no? And so I thought. With about a foot between them, my tiny-sized friend and this large stranger began this seemingly unending, and surprisingly well-coordinated dance (or if you're an avid sports fan, picture Spud Webb desperately trying to drive on Shaq) one mirroring the others' movements, swaying back and forth, side to side. Both were a bit confused as to which direction to settle on, and for an estimated 5 seconds I stood there in utter disbelief, witnessing this extremely awkward, yet ridiculously entertaining situation.

How do we avoid catastrophes like this from happening on a daily basis? And if navigating through a mall corridor without incident is THAT difficult, how does the multitude of pedestrians in somewhere like Manhattan manage to avoid such annoying or, in my friend's case, embarrassing encounters? Inattention and "mind-blindness", an inability to develop an awareness of what is in the mind of another human, would seem to be the main culprits. However, there's bit more to it than that and it involves eye gazing.

Nummenmaa, Hyona, and Hietanen over at the University of Tampere in Finland have further shed light on the science of oculomotor activity while walking. In their paper, published in the most recent issue of Psychological Science, they investigated how participants predicted where an oncoming pedestrian was going to move by using information found in that pedestrian's gaze. More specifically, they wanted to test whether humans use others' gaze information to avoid collisions during locomotion and to assess how ones' own gaze direction is influenced by the approaching pedestrian's gaze behavior.

The researchers had 35 university student participants view a computer generated male walking toward them either looking to the particpants' left or right. The scene also moved constantly forward, giving the participants the impression that they were moving. Eye movements were recorded with a digital eye tracker. The participants were to answer whether they would skirt the pedestrian by moving to the left or right using a differential button press.

Is it just me or does this guy look like he's about to do something extremely shady? (click image to enlarge)

They found that the frequency of skirting to the left was higher when the oncoming pedestrian looked to the right and conversely, skirting to the right was higher when the pedestrian looked to the left. Additionally, they found that on average the participants looked toward the opposite direction of the pedestrian's gaze. It makes sense that one would "mind read" the oncoming pedestrian traffic and focus on walking toward the path of least resistance.

Nummenmaa and her colleagues speculate that parallel mechanisms guide gaze following. One mechanism is rapid and stimulus driven while the other is slower and governed by social cognition. Interestingly enough, they referenced prior research done on autism spectrum disorders to validate this dual-system model. Individuals with autism typically have no difficulties discriminating other people's gaze direction, but exhibit impairment in both joint attention and inferring other people's mental states through gaze (due to lack of a theory of mind or ToM).

I found an additional fMRI study discovering autistic participants lack of modulation in the superior temporal sulcus, a brain area important in the processing of intentional gaze shifts (Pelphrey, Morris, & McCarthy, 2005). There's also been research looking at the pedestrian patterns of individuals with autism using virtual technology. Parsons, Mitchell, and Leonard (2004) found that a subset of autistic participants were significantly more likely to be judged to have bumped into or walked between virtual characters compared to a control group. The strange tendency couldn't be explained by executive dysfunction or general motor difficulty, suggesting that personal space may be impaired with autism. Recently, efforts have been implemented to train autistic adolescents using the same virtual technology (Mitchell, &amp, & Leonard, 2007)

However, for the rest of us who aren't diagnosed with an autism spectrum disorder, there's still a possibility we may not be utilizing our fully intact eye gazing mechanisms to "pedestrianize" properly. I can't count how many times I've seen here in the Big Apple the obnoxiously loud cellphone user or the texting pedestrian needlessly holding up foot traffic (Seriously?! Find a dark narrow alleyway or something!)

Anyway...there's this iPhone app out called "Type n Walk". New York Times has good coverage on it explaining that "it’s supposed to make it easier to text while strolling by providing a visual, on the phone, of what is happening on the street a few feet ahead". I don't really buy into it because I don't think people are that good at multi-tasking just yet (unless you're a dual-tasking meditation master). This is a prime example of how our limited brain capacity fails to keep up with the rapidly developing human computer interaction technology (props to my older brother, Gene, for making this field more congruent with our realistic cognitive abilities).

Nummenmaa and company conclude the results from their study "show that people are also aware of how and why others update their visual representations and use this information flexibly for their own movement planning and visual sampling of the environment". Unfortunately, we're unable do this if we're too busy reading or texting while walking. Furthermore, other pedestrians won't be able to tell where we're planning on going either.

So for the 67% of respondents from my survey who answered that they definitely spend more face-to-face time with a screen than with a human face, get off that Blackberry/iPhone and pay attention to where you're walking! Otherwise, CRASH.

The famous Shibuya, Japan crosswalk! It's not as tough as it looks.

Nummenmaa L, Hyönä J, & Hietanen JK (2009). I'll Walk This Way: Eyes Reveal the Direction of Locomotion and Make Passersby Look and Go the Other Way. Psychological science : a journal of the American Psychological Society / APS PMID: 19883491

Pelphrey, K. (2005). Neural basis of eye gaze processing deficits in autism Brain, 128 (5), 1038-1048 DOI: 10.1093/brain/awh404

Mitchell P, Parsons S, & Leonard A (2007). Using virtual environments for teaching social understanding to 6 adolescents with autistic spectrum disorders. Journal of autism and developmental disorders, 37 (3), 589-600 PMID: 16900403

Parsons, S., Mitchell, P., & Leonard, A. (2004). The Use and Understanding of Virtual Environments by Adolescents with Autistic Spectrum Disorders Journal of Autism and Developmental Disorders, 34 (4), 449-466 DOI: 10.1023/B:JADD.0000037421.98517.8d

The power of prediction reduces activation in the primary visual cortex

2010-02-25T14:31:00.051-05:00

Prediction is an invaluable skill for navigating through complex environments. Somehow the brain generates predictions about perceptual inputs it's likely to receive using contextual information from recent memory. Statistical regularities are learned (e.g. movement and attack patterns of Mega Man bosses) and lead to less activation in corresponding brain areas. The brain is truly a miserly organ. "Why put in more work than I have to when I know what's gonna happen next", says the brain.

Alink and colleagues over at the Max Planck Institute in Germany decided to check out what's really going on in the brain when it's making visual predictions.

Using fMRI, the team tested whether predictability reduced responses in the human visual cortex as put forth in Rao and Ballard's 1999 model of predictive coding. They assessed the theoretical claim by looking at the response of V1 (primary visual cortex) when detecting predictive and non-predictive motions.

In the first experiment the researchers had 12 healthy participants fixate their eyes on a screen during which 9 degree bars were presented above and below the fixation point. The bars induced an upward and downward long-range apparent motion. Their motions were either predictable (bar is positioned and timed exactly on the motion trajectory of linear apparent motion between the lower and upper bar stimuli) or unpredictable (bar appears at a time at which linear apparent motion had already passed the position of the test bar). A baseline condition was also presented where apparent motion, but no bar was presented. There were 81 trials for each condition, each trial lasting 7 seconds.

The second experiment differed in that the participants saw dots rather than bars through hi-tech MRI compatible goggles with two organic light-emitting diode displays. Presenting the MR Vision 2000 Ultra:

MR Vision 2000 Ultra is an excellent way of entering the world of visual stimulation for fMRI. Featuring dual, backlit digital displays, MR Vision 2000 avoids gross pixellation, pixel dropout and color aberration endemic to fiber-optic based systems...The lightweight, headmounted display fits entirely inside the bore of the magnet and is capable of deliveringfield-sequential 3D or standard video at a resolution of 180,000 pixels. This breakthrough advance utilizes the same cutting-edge technology that was developed for our research-proven fMRI 3D Goggle systems. Now its possible to immerse your patients in breathtaking 3D video! (I can't seem to find pictures of this contraption anywhere)

The authors indeed found that in both experiments the stimulus predictability reduced activation levels in V1. The first experiment showed that stimuli with a predictable onset caused lower activation of V1 compared to identical stimuli with unpredictable onset. Experiment 2 showed that responses in V1 and the hMT/V5+ (human visual motion area) were lowest when apparent motion predicted the direction of random dot motion. Visual responses increased as the motion was made less predictable.

Unfortunately, due to crappy fMRI temporal resolution, they couldn't figure out whether reduced activations in V1 were the result of feedback, local V1 processing, or an interaction between the two.

They conclude that their findings "provide strong empirical evidence for the idea that the visual cortex actively anticipates its visual input and that such anticipation allows predictable stimuli to be processed with less neural activation at the earliest cortical relay for visual processing".

As I was reading this paper, I was reminded of the neural efficiency hypothesis where more intelligent people were found to have less activation of cortical areas when performing cognitively easy tasks compared to their less intelligent counterparts. I can't shake the idea that the power of prediction is somehow inextricably tied to intelligent life. Seems to intuitively make sense doesn't it? The better the ability to accurately predict -> the better the planning -> the less likely to get zapped by a raygun.

Bet you can't beat that pesky Bubble Man as fast as I can!

Alink, A., Schwiedrzik, C., Kohler, A., Singer, W., & Muckli, L. (2010). Stimulus Predictability Reduces Responses in Primary Visual Cortex Journal of Neuroscience, 30 (8), 2960-2966 DOI: 10.1523/JNEUROSCI.3730-10.2010

Doppelmayr M, Klimesch W, Sauseng P, Hödlmoser K, Stadler W, & Hanslmayr S (2005). Intelligence related differences in EEG-bandpower. Neuroscience letters, 381 (3), 309-13 PMID: 15896490

A young Stephen Hawking

2010-02-23T22:18:00.006-05:00

I discovered this picture online of a young Stephen Hawking with his first wife Jane. When asked why she would marry a man with a 3 year life expectancy she answered,"those were the days of atomic gloom and doom, so we all had a rather short life expectancy."

more on Stephen Hawking

DSM-V Draft

2010-02-13T12:10:00.007-05:00

Finally, the draft of the DSM-V is out! They've made a few substantial changes such as the tacked on dimensional component to Axis I disorders. Although it hasn't fully moved from categorical to dimensional I suppose it's still a work in progress.

Mindhacks has written up a good summation of the key alterations. The link to the DSM-V draft can be found HERE. Explore and enjoy!

Remembering returns brain states to when the actual experience happened

2010-01-30T14:28:00.014-05:00

William James, the influential American philosopher and psychologist of the late 1800's argued that remembering events reactivated motor and sensory brain regions involved during the original event. How right he was! Danker and Anderson have written an extensive review of the research literature looking at how this all happens, cleverly titled "The Ghosts of Brain States Past". Here is there abstract from the latest issue of Psychological Bulletin.

There is growing evidence that the brain regions involved in encoding an episode are partially reactivated when that episode is later remembered. That is, the process of remembering an episode involves literally returning to the brain state that was present during that episode. This article reviews studies of episodic and associative memory that provide support for the assertion that encoding regions are reactivated during subsequent retrieval. In the first section, studies are reviewed in which neutral stimuli were associated with different modalities of sensory stimuli or different valences of emotional stimuli. When the neutral stimuli were later used as retrieval cues, relevant sensory and emotion processing regions were reactivated.

In the second section, studies are reviewed in which participants used different strategies for encoding stimuli. When the stimuli were later retrieved, regions associated with the different encoding strategies were reactivated. Together, these studies demonstrate not only that the encoding experience determines which regions are activated during subsequent retrieval but also that the same regions are activated during encoding and retrieval. In the final section, relevant questions are posed and discussed regarding the reactivation of encoding regions during retrieval.

Some interesting points about brain region reactivation:

1. reactivation of the visual system occurs at the multi-granular level
2. reactivation is stronger during retrieval of more info
3. there's a reduction in reactivation when info is falsely remembered
4. reactivation is correlated with subjective reports of remembering (a bit surprising given how fallible our memories often are)

The authors conclude by asking whether reactivation of brain states are more easily activated when info is more accessible. What about the role of speed and other varying factors? All of these questions, I am sure, will be answered before we forget.

Danker, J., & Anderson, J. (2010). The ghosts of brain states past: Remembering reactivates the brain regions engaged during encoding. Psychological Bulletin, 136 (1), 87-102 DOI: 10.1037/a0017937

I think, therefore I dream

2010-01-23T10:02:00.011-05:00

I woke up late last night experiencing first-hand the production of my dreams; these intimate yet ephemeral narratives fabricated by the brain to explain its very own workings...better yet, its very own existence.

Can distractions really enhance motor performance?

2010-01-19T21:55:00.027-05:00

Texting while driving seems to score pretty high up there on the "I really shouldn't be doing this right now" list.

A study in 2009 by the Virginia Tech Transportation Institute found that truck drivers who were texting on the road were 23 times more likely to find themselves involved in an accident.

Incidentally, and much to my bewilderment, truck drivers who talked on cell phones were found to have absolutely no increased risk for crashing. I suppose it's much easier to say over the phone than to text "Slow down. Smokey Bear (cop) on your tail. Watch out for that barbershop (bridge lower than 13'6") up ahead or you'll soon find yourself driving a bobtail (tractor without a trailer). Looks about time to head over to that pickle park (a state highway rest area...I wonder why they call it that...)". You can find more CB terminology here.

Most of us would likely think any type of distraction would negatively affect motor performance. However, a recent study by Hemond, Brown, and Robertson published in the Journal of Neuroscience, proves this isn't necessarily the case.

The team from Harvard Medical School and McGill University questioned whether the very nature of the distraction would play a role in motor performance by either impairing or enhancing performance. They had a total of four conditions. In condition 1 they had participants complete a task involving motor and color sequencing; the color sequencing serving as a distraction. In condition 2, participants performed both a sequencing and counting task; the counting serving as a distraction. Condition 3 was a randomly assorted task while condition 4 involved a motor sequencing task without distraction.

They found that learning of a motor sequencing task can be enhanced by concurrently performing another sequencing task (condition 1). In contrast, learning was impaired when performance of concurrent tasks did not involve the same cognitive processes (condition 2).

So it's really not about the complexity of information which determines performance, but more about the processes engaged and whether they are similar or different. This led me to wonder what effects intensive simulated training would have on performance. A study done in 1998 by Regan, Deery, and Triggs over at Monash University Accident Research Centre in Australia addressed this very thought quite nicely.

In one of their experimental conditions they had participants (novice drivers) complete numerical calculations while concurrently performing a simulated driving task. The numerical calculation task consisted of a single digit appearing in front of the driving participants for one second every five seconds. The participants were required to calculate the difference between the previous two numbers and answer whether the derived number equaled the currently displayed number. They then responded yes or no by pressing one of two switches located on the steering wheel. Training consisted of 20 trials at two minutes each trial.

The authors found that the training group indeed performed better on the driving task compared to a control group. However, the control group tended to do a bit better on the numerical calculation task, although non-significantly. The conclusions of this particular study suggests that training may enhance attentional control while driving. However, this by no means condones the act of texting while driving, even if one were to train for hours on end.

The take home message here folks is to text while you're blogging, not while you're driving!...unless of course, you're already reading road signs. I kid.

Reagan, M. A., Deery, H. A., & Triggs, T. J. (1998). Simulator-based training of attentional control skill in novice drivers. SimTecT98

Hemond, C., Brown, R., & Robertson, E. (2010). A Distraction Can Impair or Enhance Motor Performance Journal of Neuroscience, 30 (2), 650-654 DOI: 10.1523/JNEUROSCI.4592-09.2010

Anticipating reward improves learning during sleep

2010-01-04T23:32:00.022-05:00

Rocking out on the guitar is by far one of my most cherished pastimes. At the angst ridden age of 15 I picked up a cheap Ibanez strat and learned my very first Nirvana song, "Teen Spirit". Little did I know a good night's rest would play such a crucial role in my learning those simple power chords. Furthermore, who would've thought my desire to become the next grunge icon would determine the rate at which I learned during those quiet nights of sleep.

According to a study by Fischer and Born, published in the most recent journal of SLEEP, they found that merely anticipating a reward can determine the amount of memory consolidation during those important times of offline processing.

The authors split up 76 adult subjects (20-33) into wake and sleep groups. All subjects learned a finger sequence tapping task with their non dominant hand and all subjects except for the control groups were told that additional payment would be contingent upon their improvement after the retention interval (12 hrs).

Results showed that overall motor skill improvement was seen exclusively in the sleep condition. Furthermore, they found that sleep induced a significant improvement that was associated with the anticipated reward before the retention interval compared to the nonreward associated sequence. However, the authors note that circadian factors and mental rehearsal during retention could've partially confounded their findings.

So for all the future professional finger tappers out there, get that sleep, but make sure to really believe you'll be greatly rewarded for your unrelenting efforts.

Fischer S, & Born J (2009). Anticipated reward enhances offline learning during sleep. Journal of experimental psychology. Learning, memory, and cognition, 35 (6), 1586-93 PMID: 19857029

Can modern day gadgets help combat prejudice?

2009-12-22T20:15:00.084-05:00

Prejudice...we've all experienced it at one point or another. Defined as a preconceived belief, opinion, or judgment toward a group or person because of race, social class, gender, ethnicity, sexual orientation, etc., it also means a priori beliefs that include any unreasonable attitude that is unusually resistant to rational influence.

It's been the cause of countless wars and an infinite amount of unnecessary suffering. It must be put to an end once and for all! But first we must look at the underlying mechanisms that continue propagating such maladaptive cognitions and behaviors. So how do today's researchers go about investigating prejudice anyway?

Cunningham, et. al (2004) used the Implicit Association Online Test (https://implicit.harvard.edu/) developed by Greenwald in 1998 to measures unconscious prejudice of certain groups. Subjects had to pair groups with "good" and "bad" labels and were given only a fraction of a second to respond; a mere gut reaction. From 1998 to now 2.5 million tests have been taken. Findings showed strongest prejudice against the elderly. There was less shame concerning bias against gays/lesbians and the obese.

Banaji, a colleague of Cunningham's, showed in 2003 that when white students consciously recognized black faces brain areas involved with controlled thinking became active. Rational thought was triggered. Subjects were given the opportunity to challenge their implicit prejudice in this gut reaction free condition. She states "the imprint of culture is what we see in the subliminal exposure".

As the original developer of the Implicit Association Test, Greenwald et. al (2003) decided to take a further look at the prejudice happening all around us. He asked whether police officers, looking out for criminal activity, would lead to them focus more on black faces than white faces. He used a pseudo virtual reality experiment where subjects were asked to either fire at or not fire at simulated criminals (with guns), police officers (with guns), or citizens (with harmless objects). Findings showed that this indeed proved to be the case.

Dotsch and Wigboldus (2007) investigated how prejudiced implicit associations affected physiological and behavioral responses. Subjects were immersed in a virtual environment where they encountered either a White or Moroccan avatar. Results showed that subjects maintained further distance and showed increase in skin conductance levels (fear response) when approaching Moroccan avatars as opposed to White avatars.

Harris and Fiske (2007) looked at social groups that elicit disgust (e.g. homeless people, drug dealers) and found that they were processed differently in the medial prefrontal cortex (mPFC), a brain area crucial for social cognition. Lower activation of the mPFC could mean that these groups were being perceived as less than human.

Here's an fMRI of the subjects' brain activity (yellow circle=social emotion (in group), red circle=non-social emotion (out group)):

So if all these healthy people are responding in prejudice ways that seem almost automatic, could it mean that prejudice is innate, ingrained through years of evolutionary process? Tribal psychology suggests that it's a strategy that enhances individual survival. There's not enough time to form legitimate views about potential threat so an innate response would be to defend against the "other".

Olsson, in 2005 decided to further probe this question and specifically asked whether humans were genetically predisposed to be racists. She found that fear conditioning extend to social groups defined by race. Results indicated that individuals from a racial group other than one's own were more readily associated with an aversive stimulus than individuals of one's own race, among both white and black subjects.

So is it a matter of preparedness? Not likely according to Maia (2009). She re-interpreted Olsson's findings by first explaining that the timing and pattern of differentiation of human ‘‘races'' made it unlikely that humans could have evolved mechanisms specifically to learn to fear different races. Additionally, human populations differentiated into different races relatively recently in evolutionary history where different groups evolved different characteristics because they were relatively isolated from each other. So being genetically prepared to fear individuals from different races was unlikely to have provided any selective advantage. So in fact it’s really about familiarity and exposure not evolution. IT’S LEARNED!

If being prejudiced is a learned trait, then how do we unlearn it? Allport, in 1954 came up with this nifty theory termed the Contact Theory as a reaction to WWII. Basically he purported that given the right conditions if members of differing groups come in contact with one another, the interaction ultimately leads to more positive intergroup relations. The theory has been slightly modified over the years but here's an overall diagram of what the model looks like.

Crisp and Turner(2009) asked whether imagined interactions produce positive perceptions? They found that simply imagining a positive social interaction with an “outgroup” improved intergroup attitudes, greater projection of positive traits to outgroups, reduced anxiety, and reduced stereotype threat. Examples were changing of young people's attitudes toward older people, straight men's attitudes toward gay men, and Mexican people's attitudes toward Metizos in Mexico. They ruled out cognitive load, demand characteristics, stereotype priming, and positive affect as possible alternative explanations.

If the power of imagination is so effective could virtual reality take this concept of Contact Theory one step further? Groom, Bailenson, & Nass (2009) asked the very same question. They investigated how people’s implicit racial bias was affected by the race of their avatar in an immersive virtual environment.

The fascinating study consisted of 98 Undergraduate students shown either picture of a black or white person. They were asked to “imagine a day in the life of” the person they were shown and told they would be later interviewed as that person. They then proceeded to put on virtual gear and looked into a virtual mirror (i.e. embodiment of a black avatar, white avatar, or empty mirror control condition). Afterward, they went on a virtual job interview in which confederate interviewer was blind to subject’s virtual race. After completion, subjects filled out Implicit Association Test and measures of explicit racial bias.

The authors found that people’s implicit racial bias varied depending on the model race they embodied. The imagined condition showed no significant difference between white and black models. Surprisingly, subjects embodied by black avatars showed greater racial bias favoring whites compared to subjects embodied by white avatars. They suggested that people aware of stereotypes expressed implicit bias when stereotypes were activated (i.e. looking at the black avatar in the mirror). They concluded that results do not support the perspective taking theory and indicate that automatic racial bias is NOT reduced by embodying a disfavored racial group.

Another strike against using virtual reality to combat the evils of prejudice is the fact that a strange phenomena exists termed the Uncanny Valley. It's basically when robots and other facsimiles of humans look and act almost like actual humans where it causes a response of revulsions among human observers.

This construct originally developed by Masahiro in 1970, explains that the "valley" in question is a dip in a proposed graph of the positivity of human reaction as a function of a robot's life-likeness. Some funny clips to illustrate what I'm talking about.

Hilarious clip from 30 Rock further explaining the phenomena using Star Wars characters! http://kotaku.com/384789/the-uncanny-valley-explained-in-terms-of-porn-and-star-wars

Steckenfinger and Ghazanfar (2009) found that even monkeys preferred looking at real and unrealistic synthetic faces as opposed to real synthetic faces.

Some popular theories of why the Uncanny Valley exists include mate selection, automatic stimulus driven appraisals of uncanny stimuli elicit avoidance of unhealthy mate, pathogen avoidance, categorizing difficulties, and a violation of human norms.

If something as sophisticated as virtual reality won't work then what will? It seems like it's time to go back to the basics. Mirrors my friends!!! MIRRORS!

Wiekens and Stapel (2008) in an ingenious experiment investigated whether the presence of mirrors effected levels of prejudice. In the first of two experiments they had 164 students from Holland assigned to a mirror condition (filling out questionnaire in the presence of a mirror) or scanning for first person pronouns condition. Both conditions increased private self-awareness, but only the mirror condition additionally increased public self-awareness.

In the second experiment 127 students from Holland were asked to positively or negatively rate a Surinamese man (ethnic minority in Holland) after reading an ambiguous story of him. They were then assigned to either the first person pronoun, mirror, or control condition.

The authors found that students revealing prejudice in an earlier questionnaire were more likely to negatively rate the Surinamese man after completing the pronoun task compared to controls who didn’t perform the task. They also found that students who sat in the presence of a mirror were less likely to rate the Surinamese man in a negative way, compared with control students who didn't have a mirror near them.

Conclusion: MIRRORS WORK! (except for virtual reality mirrors apparently)

Maybe...just maybe with the placement of more mirrors within the public sphere, opportunities for nonjudgmental and open exchange between differing groups will begin to flourish.

In the words of the famous actor/comedian W. C. Fields, "I'm free of all prejudices. I hate everyone equally”.

This just in. HP computers are racist...

References:
Crisp, R., & Turner, R. (2009). Can imagined interactions produce positive perceptions?: Reducing prejudice through simulated social contact. American Psychologist, 64 (4), 231-240 DOI: 10.1037/a0014718

Cunningham, W., Johnson, M., Raye, C., Chris Gatenby, J., Gore, J., & Banaji, M. (2004). Separable Neural Components in the Processing of Black and White Faces Psychological Science, 15 (12), 806-813 DOI: 10.1111/j.0956-7976.2004.00760.x

Greenwald, A. (2003). Targets of discrimination: Effects of race on responses to weapons holders Journal of Experimental Social Psychology, 39 (4), 399-405 DOI: 10.1016/S0022-1031(03)00020-9

Groom, V., Bailenson, J.N., & Nass, C. (2009). The influence of racial embodiment on racial bias in immersive virtual environments. Social Influence, 4, 1-18.

Harris, L., & Fiske, S. (2006). Social groups that elicit disgust are differentially processed in mPFC Social Cognitive and Affective Neuroscience, 2 (1), 45-51 DOI: 10.1093/scan/nsl037

Olsson, A. (2005). The Role of Social Groups in the Persistence of Learned Fear Science, 309 (5735), 785-787 DOI: 10.1126/science.1113551

Steckenfinger SA, & Ghazanfar AA (2009). Monkey visual behavior falls into the uncanny valley. Proceedings of the National Academy of Sciences of the United States of America, 106 (43), 18362-6 PMID: 19822765

Tiago V. Maia (2009). Fear Conditioning and Social Groups: Statistics, Not Genetics Cognitive Science, 33, 1232-1251.

Wiekens, C., & Stapel, D. (2008). The Mirror and I: When private opinions are in conflict with public norms Journal of Experimental Social Psychology, 44 (4), 1160-1166 DOI: 10.1016/j.jesp.2008.02.005

So we've figured out memory huh?

2009-12-16T17:15:00.009-05:00

A snippet of the article from Science Daily documenting Tsien's work:

"It's a beginning, a first glimpse of a memory," Dr. Tsien said.

"For the first time it gives us the ability to look at the brain dynamic and tell what kind of memory is formed, what are the components of the memory and how the memory is retrieved at the network level." The finding could help pinpoint at what stage memory formation is flawed and whether drugs are improving it...A computational algorithm translated the neuronal chatter into a discernable and dynamic activity pattern that provided scientists a trace or picture of what the memory looked like as it was formed and recalled.

http://www.sciencedaily.com/releases/2009/12/091215202322.htm

Posts that caught my eye and prolonged procrastination

2009-12-02T20:51:00.007-05:00

Neurocognitive processes of the religious leader in Christians.

Experts: Man controlled robotic hand with thoughts
LOL...obscene gestures with a robotic hand?

Talks Pranav Mistry: The thrilling potential of SixthSense technology
All I can say is wow.

http://thebrainobservatory.ucsd.edu/hm_live.php
I find the monotonous slicing of H.M.'s brain somewhat hypnotic in nature.

The Brain The Big Similarities & Quirky Differences Between Our Left and Right Brains
Makes you think about the true potential of the human brain.

Music, musicians, and the brain: an exploration of

musical genius

If only I had absolute pitch...

How Your Brain Grows From A Sensory to A Cognitive World

No way Susan Greenfield...I have not blown away my mind with "techno techno techno". Great lecture though.

FROM JACKSON POLLOCK TO JOHN COLTRANE — HOW CREATIVITY SPRINGS FROM A CHOREOGRAPHED SET OF MENTAL EVENTS.

An oldie but goodie...i love jazz! (except for the super abstract kind i.e. 20 minute bongo solo)

Genes Don't Make You Racist

The somniloquy hypothesis: How the immature brain learns facts

2009-11-17T00:53:00.039-05:00

A while back I wrote about the possible adaptive function of somnambulism or sleep-walking. Well...I've come up with yet another hypothesis addressing an "abnormal" behavior falling under parasomnias.

Somniloquy or sleep-talking can happen during stages of REM or NREM sleep (I'm speaking to the latter). This seemingly bizarre behavior typically occurs in childhood and is outgrown by puberty. Presentation can vary from rhythmic nonsense words to long coherent speeches. No one really knows where it comes from. The most popular answer seems to be because of stress.

We could just leave it at that, but it doesn't really explain why the behavior came about in the first place (plus stress seems to play more of a role in REM somniloquy anyway). I have a hard time simply writing-off weird behaviors that have managed to stick around for long periods of time. In my head I'm thinking "there's just gotta be a functional purpose"!

Here's what I think NREM sleep-talking is all about. Many studies have shown that NREM sleep is where declarative memory (i.e. factual knowledge) is consolidated (Backhaus et. al, 2006, Daurat, Terrier, Foret, & Tiberge, 2007, Gais, & Born, 2004, Tucker et. al, 2006, Wagner, & Born, 2008). The presence of somniloquys is just evidence of this. It's a sign that the maturing brain is rehearsing and consolidating syntactic and semantic bits of information.

It's important to note that the calm quality of NREM sleep-talk is very different compared to the loud and emotional sleep-talk found during rapid eye movement behavior disorder. This makes a lot of sense. REM sleep is known to process emotional memory so of course you'd see this kind of late night emotionally charged verbal diarrhea. Some have postulated that this erratic unconscious behavior protected the stressed out sleep deprived caveman from hungry predators looking for some easy eats.

On the flip side, factual bits of data like "Paris is the capital of France" isn't emotional at all (unless you're strangely disturbed by this bit of info) and that's why you hear the flat affect during NREM somniloquy.

So there you go. I've laid out a tentative explanation for NREM somniloquys. I haven't seen anything else out there to explain this more pleasant form of sleep-talking (if do you spot any please let me know). However, the only way to really prove my hypothesis is by figuring out a way to induce somniloquys in different stages of sleep while observing the activity of the brain.

In the meantime, I wouldn't fret too much over your kids mumbling in their sleep something about world domination. They're probably just learning how to orate more effectively.

Gais S, & Born J (2004). Declarative memory consolidation: mechanisms acting during human sleep. Learning & memory (Cold Spring Harbor, N.Y.), 11 (6), 679-85 PMID: 15576885

Petit, D., Touchette, E., Tremblay, R., Boivin, M., & Montplaisir, J. (2007). Dyssomnias and Parasomnias in Early Childhood PEDIATRICS, 119 (5) DOI: 10.1542/peds.2006-2132

Backhaus J, Junghanns K, Born J, Hohaus K, Faasch F, & Hohagen F (2006). Impaired declarative memory consolidation during sleep in patients with primary insomnia: Influence of sleep architecture and nocturnal cortisol release. Biological psychiatry, 60 (12), 1324-30 PMID: 16876140

Daurat A, Terrier P, Foret J, & Tiberge M (2007). Slow wave sleep and recollection in recognition memory. Consciousness and cognition, 16 (2), 445-55 PMID: 16877007

Tucker MA, Hirota Y, Wamsley EJ, Lau H, Chaklader A, & Fishbein W (2006). A daytime nap containing solely non-REM sleep enhances declarative but not procedural memory. Neurobiology of learning and memory, 86 (2), 241-7 PMID: 16647282

Wagner, U., & Born, J. (2008). Memory consolidation during sleep: Interactive effects of sleep stages and HPA regulation Stress, 11 (1), 28-41 DOI: 10.1080/10253890701408822

The dual-tasking meditation master

2009-11-12T01:30:00.008-05:00

I recently read an article in the latest Scientific American Mind magazine discussing the cell mechanisms underlying meditative states. The author briefly mentioned the fact that expert meditators were able to avoid the attentional blink that lay people are prone to experiencing when barraged with rapidly presented visual stimuli.

This brought up a question for me. Would expert meditators perform better on dual-tasks compared to age-matched subjects?

I believe the answer is in the affirmative. My reasoning behind this hypothesis has to do with the fact that meditation not only strengthens attentional abilities, but fosters neural efficiency as well (dual-tasking is not about doing two things simultaneously, but more about doing one thing at a time at an extremely fast pace, thus creating an illusion as if one is doing two things at once). A 2007 study by Farb et. al has shown that meditation activates the anterior cingulate cortex, which is a region central to switching your attention.

With the development of my dual-task paradigm underway I hope to prove that daily meditation practice can have beneficial effects when it comes to multi-tasking. If my prediction proves to be true, not only will this ancient practice developed thousands of years ago better our physical and emotional well-being, but assist us in keeping afloat in this fast pace era of "divided attention" as well.

Farb, N., Segal, Z., Mayberg, H., Bean, J., McKeon, D., Fatima, Z., & Anderson, A. (2007). Attending to the present: mindfulness meditation reveals distinct neural modes of self-reference Social Cognitive and Affective Neuroscience, 2 (4), 313-322 DOI: 10.1093/scan/nsm030

The Orchid Hypothesis

2009-11-10T23:17:00.007-05:00

I must say this is by far one of the most informative and exciting entries I've read all year. Dobbs does a good job explaining the more promising alternative to the diathesis-stress model.

Most of us have genes that make us as hardy as dandelions: able to take root and survive almost anywhere. A few of us, however, are more like the orchid: fragile and fickle, but capable of blooming spectacularly if given greenhouse care. So holds a provocative new theory of genetics, which asserts that the very genes that give us the most trouble as a species, causing behaviors that are self-destructive and antisocial, also underlie humankind’s phenomenal adaptability and evolutionary success. With a bad environment and poor parenting, orchid children can end up depressed, drug-addicted, or in jail—but with the right environment and good parenting, they can grow up to be society’s most creative, successful, and happy people.

I highly suggest checking it out:

http://www.theatlantic.com/doc/200912/dobbs-orchid-gene

Neuroscience and free will

2009-11-06T15:53:00.002-05:00

This video speaks briefly to my previous post on free will. Enjoy!

Stimulating the nucleus accumbens may help the severely depressed

2009-11-02T19:26:00.002-05:00

http://www.alphagalileo.org/ViewItem.aspx?ItemId=62473&CultureCode=en

2009-11-01T14:51:00.004-05:00

Am I conscious now?

-Susan Blackmore

http://www.oneworld-publications.com/site07/misc/Am_I_conscious_now_Short.mp3

Screen time poll

2009-10-30T02:07:00.011-04:00

I've come to the realization that I spend more time interacting with a screen than I do interacting with real human faces...I wonder if others feel the same way? If this is true for the most of us out there what does it mean for the evolution of our brains? What does it mean for the future of humanity? Wall-E in the making?

The curious case of H.M.

2009-10-25T02:17:00.033-04:00

Recently, I watched a lecture by the renown neuroscientist, Eric Kandel, on Youtube. In his talk he unsurprisingly made mention of the famous patient H.M. in which most of us are familiar with. I've always been curious as to who the person was behind the famous initials. What did he/she look like? What were some of his/her hobbies? To those who were also curious but never had a chance to find out, here he is...the man, the myth, the legend.

Henry Gustav Molaison

February 26, 1926 – December 2, 2008

Henry's favorite past times were crossword puzzles, playing bingo, watching TV, and socializing with his caretakers.

It's funny how a person who revolutionized the field of neuroscience wasn't even a neuroscientist.

Thank you Henry for your significant contribution to the study of memory. You will never be forgotten.

New York Time's obituary

Wikipedia entry

More pictures

Optogenetics FTMFW!

2009-10-19T21:30:00.009-04:00

Optogenetics is an emerging field combining optical and genetic techniques to probe neural circuits within intact mammals and other animals, at the high speeds (millisecond-timescale) needed to understand brain information processing.

All your brain are belong to us.

Learn more about optogenetics with these links:

http://en.wikipedia.org/wiki/Optogenetics

http://www.wired.com/wiredscience/tag/optogenetic/

http://www.laboratoryequipment.com/News-remote-control-flies-101909.aspx?xmlmenuid=51

http://biox.stanford.edu/biox/optogenetics.html

More or less conscious

2009-10-18T11:34:00.005-04:00

Are Alzheimer patients less conscious than healthy individuals? This would be true if we were to assume Chalmer's suggestion, that functional organization determines higher levels of consciousness, was correct. Just a thought...

Are they conscious or not?

2009-10-15T10:09:00.011-04:00

I apologize for the lack of posts as of late. I've been putting in ridiculous hours over at school.

In any case, I recently stumbled upon Joshua Knobes' blog entry over at Experimental Philosophy summarizing Felipe De Brigard's fascinating paper forthcoming in the Journal of Consciousness Studies. De Brigard found that simply framing a question in a certain way can determine whether a person is perceived to be conscious or not. The link can be found here.

Aaah...the power of questions...back to the dungeon I go.

Children recruit higher-order brain mechanisms during a numerical comparison task

2009-10-05T13:07:00.020-04:00

I've been endlessly scoring digit-symbol coding protocols (fun...), a subtest of the WAIS-IV measuring working memory, for the past few weeks at my new neuropsych externship so the following article seems particularly relevant.

In a recent study by Cantlon and colleagues published in the latest Journal of Cognitive Neuroscience, they decided to measure the brain activity of 6-7 year-old children during numerical comparison tasks using fMRI.

An example of a numerical comparsion task:

...participants were required to compare a single digit Arabic number presented on the center square with the standard, 5. Participants were asked to reach and touch one of three squares on the screen with their index finger while their hand movement trajectories were recorded: the left square for 1–4, the center for 5, and the right for 6–9 (Song & Nakayama, 2007).

The authors found that 6- and 7-year-old children recruit the occipito-temporal and parietal cortex in order to solve numerical comparisons across different notation systems, similar to that of adults. However, (here's the kicker) the fMRI showed that children also activate the inferior frontal cortex to a much greater degree than adults during these numerical comparison tasks. This particular area of the brain involves Brodmann area 44 and 45, used for retrieving semantic information when strong stimulus-stimulus associations are absent.

Interestingly enough, the inferior frontal cortex has also been shown to play a role in music cognition (Levitin, 2009). Could kindergarten be the optimal time to learn how to play an instrument?

The current study provides further evidence that "a core neural system integrates notation-independent numerical representations throughout development but, early in development, higher-order brain mechanisms mediate this process".

Song JH, & Nakayama K (2008). Numeric comparison in a visually-guided manual reaching task. Cognition, 106 (2), 994-1003 PMID: 17512516

Levitin, D. (2009). The Neural Correlates of Temporal Structure in Music Music and Medicine, 1 (1), 9-13 DOI: 10.1177/1943862109338604

Cantlon, J., Libertus, M., Pinel, P., Dehaene, S., Brannon, E., & Pelphrey, K. (2009). The Neural Development of an Abstract Concept of Number Journal of Cognitive Neuroscience, 21 (11), 2217-2229 DOI: 10.1162/jocn.2008.21159

Bye bye modular, hello cognit!

2009-09-30T00:43:00.029-04:00

What is a cognit you ask? It's a basic unit of memory or knowledge defined by pattern of connections between a network of neurons associated by experience.

Termed by Fuster in 2006, the construct was created to solve the problematic yet popular view that the human brain is made up of discrete cortical domains dedicated exclusively to visual discrimination, language, spatial attention, face recognition, motor programming, memory retrieval, and working memory.

Although the modular modeling of the brain has utterly failed due to a lack of conclusive evidence, many neuroscientists continue to maintain this antiquated view... but why? Put quite simply, there was nothing better. However, thanks to Fuster, a new paradigm is emerging...

Introducing the cognit network model. It postulates that memory and knowledge are represented by interactive, distributed, and overlapping networks of neurons in association cortices.

The posterior-post-rolandic association cortex contains perceptual cognits and the frontal association cortex contains executive cognits. The prefrontal and posterior association cortices are linked by complex cognits in a hierarchical order. The parasensory and premotor cortex, found at the bottom of the hierarchy, contain relatively simple and small cognits which represent motor acts or simple percepts. At the top of the hierarchy is the temporo–parietal and prefrontal cortex containing larger cognits representing complex and abstract information of perception and executive control. The long reciprocal cortico–cortical connections between the posterior and frontal networks support sequential behavior, speech, and reasoning.

What I find most fascinating about the whole thing is that it's possible for a single neuron to be involved in multiple memory networks thus playing a part in many memories and units of knowledge.

Fuster JM (2009). Cortex and memory: emergence of a new paradigm. Journal of cognitive neuroscience, 21 (11), 2047-72 PMID: 19485699

FUSTER, J. (2006). The cognit: A network model of cortical representation International Journal of Psychophysiology, 60 (2), 125-132 DOI: 10.1016/j.ijpsycho.2005.12.015

Why primate eyes prefer the color black

2009-09-28T07:20:00.037-04:00

A recent study by Yeh, Xing, and Shapley over at The Center for Neural Science, New York University made a fascinating discovery about the primary visual cortex of the macaque monkey and it's preference for black over white stimuli similar to that of humans. Here's a snippet from their abstract.

From recordings of single-cell activity in the macaque monkey's primary visual cortex (V1), we found that black-dominant neurons substantially outnumbered white-dominant neurons in the corticocortical output layers 2/3, but the numbers of black- and white-dominant neurons were nearly equal in the thalamocortical input layer 4c. These results strongly suggest that the black-over-white preference is generated or greatly amplified in V1. The predominance of OFF neurons in layers 2/3 of V1, which provide visual input to higher cortical areas, may explain why human subjects detect black more easily than white. Furthermore, our results agree with human EEG and fMRI findings that V1 responses to decrements are stronger than to increments, though the OFF/ON imbalance we found in layers 2/3 of macaque V1 is much larger than in the whole V1 population in the human V1 experiments (Zemon et al., 1988, 1995; Olman et al., 2008).

No wonder boldface text literally catches the eye.

Yeh CI, Xing D, & Shapley RM (2009). "Black" responses dominate macaque primary visual cortex v1. The Journal of neuroscience : the official journal of the Society for Neuroscience, 29 (38), 11753-60 PMID: 19776262

Why middle-agers shouldn't join the army

2009-09-22T18:33:00.060-04:00

Enlisting in the army is a significant life-changing decision, especially for someone who's middle-aged. Apparently there's an age cap of 42 for active duty. The reasoning behind this seemingly arbitrary number is that it allow for a 20-year military career before retirement. However, perhaps they should look toward a younger cutoff point in light of a recent study investigating the effects of sleep deprivation on arousal levels of middle-aged rats. But before we continue with this line of argument, lets define what being middle-aged really means.

According to the US Consensus middle-age ranges anywhere from 35 to 54. During this stage of life one begins to see visible signs of aging, loss of skin elasticity, and graying hair. In addition, physical fitness decreases, body fat accumulates, and a decrease in both aerobic performance and maximal heart rate ensues.

You may be asking yourself why any sane middle-aged person would ever want to enlist into the army, especially at such a physically disadvantageous age. Well...there ARE people out there who have their various reasons. One middle-ager, Russell Dilling, decided to follow through with his life-long dream and joined at the ripe age of 42 after divorcing a wife who refused to be in a military marriage. Another middle-aged aspirant of the military life posted, "I really wanted to be a cop or firefighter, but their qualifying standards are too tough. Also, cops and firefighters don't get the great benefits that military people do, like free health care, housing, discounts at the PX, job placement assistance, and various other preferential treatment", to which an incredulous military solider responded, "[I] think you have the Army mixed up with the Welfare system...". Hilarious.

In any case, it's no secret that soldiers experience long bouts of sleep deprivation during combat and perhaps even in training. This is why the U.S. military developed its very own sleep-reduction program. It seems as if the development of a drug to help cut down that pesky need for sleep is on the horizon (or already here). In an unclassified report the defense science advisory group known as JASON wrote:

[T]he maximum casualty rate depends strongly on the individual's sleep need, τ0. Hence any effort to improve human performance to minimize τ0 for given tasks can lead to a significant decrease in the casualty rate, of [about] 20 percent. … Suppose a human could be engineered who slept for the same amount of time as a giraffe (1.9 hours per night). This would lead to an approximately twofold decrease in the casualty rate. An adversary would need an approximately 40 percent increase in the troop level to compensate for this advantage.

So why might it be a bad idea for middle-aged adults to enlist into the army?

A recent study by Wigren, Rytkönen, and Porkka-Heiskanen over at the University of Helsinki investigated how aging affected the capacity of the basal forebrain (BF), a crucial area for sustaining cortical arousal, to cope with prolonged waking activity. They found that lactate, a chemical induced by neural activity, increased in sleep deprived young but not middle-aged or old rats. Additionally, they observed an attenuation of increased high-frequency (HF) EEG theta power (7–9 Hz), a marker of cortical arousal and active waking, in middle-aged and old rats.

The results suggest that age-related weakening of BF functioning reduces cortical arousal during prolonged waking. In other words, middle-aged and old rat brains just can't hang with that of their younger counterparts when it comes to sustaining wakefulness after a period of sleep deprivation. How is private Dilling going to stay awake during long hours of combat? What's even worse, sleep deprivation may reduce subsequent sleep intensity within this age group and further impair cognitive functioning (also check out how Sleep deprivation might lead to Alzheimer's).

Obviously further research on human subjects is needed before any definitive conclusions can be drawn. For now, those of you who are currently experiencing a mid-life crisis and want to prove that you've still got what it takes, I suggest avoiding enlistment and maybe purchasing a Harley motorcycle instead. Just make sure you get enough sleep before taking it out for a long cruise.

Wigren HK, Rytkönen KM, & Porkka-Heiskanen T (2009). Basal forebrain lactate release and promotion of cortical arousal during prolonged waking is attenuated in aging. The Journal of neuroscience : the official journal of the Society for Neuroscience, 29 (37), 11698-707 PMID: 19759316

Observation of tool use activates specific brain area only in humans

2009-09-18T22:14:00.048-04:00

How'd those Frosted Flakes manage to get so high up in that cabinet? Can't...reach. Aha! Stool! Argh...still no dice. Darn these short arms. Oh oh! Broom! Almost got it...almost...almost...::crash:: NOOO!!! Game Over.

The discovery that a species other than human has the ability to use tools has, quite frankly, lost its novelty. Just look at the New Caledonian crow. If trained properly, it can utilize up to three different tools sequentially to reach for a target food reward (Wimpenny et. al, 2009). It does this by first picking up a stick-like tool with its beak. It then uses this tool to retrieve a second tool which is then used to retrieve a third tool. Finally, the third tool is used to successfully retrieve the food (sadly, I couldn't even do it using two).

An earlier study conducted by Taylor et. al (2007) demonstrating how the New Caledonian crow utilizes two tools in sequential order to retrieve a food reward:

If a mere "bird brain" can manage to use tools in such a complex way what makes us so special? Is the human brain really that much more "evolved" in comparison to the brains of other animals?

A study by Peeters and colleagues published in this weeks Journal of Neuroscience may offer further clues to these questions. The researchers had a large cohort of human volunteers, untrained monkeys, and trained monkeys watch videos demonstrating hand actions and actions performed using simple tools. This led to the activation of bilateral occipitotemporal, intraparietal, and ventral premotor cortices in all groups.

However, they found that after watching the simple tool use video a rostral sector of the left inferior parietal lobule known as the left anterior supra marginal gyrus (aSMG) was activated in humans ONLY. This is a curious finding because one would think that the trained monkeys would also show similar activations in this particular area of the brain. So what does this all mean?

According to the results the human aSMG is only activated during the observation of hand grasping and not during static representation of tool images, indicating the aSMG's involvement in the cognitive aspect of tool use. The aSMG associates the intended use of the tool with the results obtained by using it.

The authors suggest that the rostral part of the IPL is a new brain area exclusive to humans and functions to understand tool actions. They note that this is indeed a "fundamental cognitive leap that greatly enlarged the motor repertoire of humans and, therefore, their capacity to interact with the environment".

They go on to state that even though monkeys know how to use tools it doesn't necessarily imply an understanding of the abstract relationship between the tools being used and the goals that can be achieved by using them. Boo-yah! In your face monkeys! It seems like we really are special...for now.

Here's a video of the fuzzy haired critters using anvils and hammers to break open some delicious snacks.

I also provide a link to Wired's Clever Critters: 8 Best Non-Human Tool Users

Wimpenny JH, Weir AA, Clayton L, Rutz C, & Kacelnik A (2009). Cognitive processes associated with sequential tool use in New Caledonian crows. PloS one, 4 (8) PMID: 19654861

Peeters R, Simone L, Nelissen K, Fabbri-Destro M, Vanduffel W, Rizzolatti G, & Orban GA (2009). The representation of tool use in humans and monkeys: common and uniquely human features. The Journal of neuroscience : the official journal of the Society for Neuroscience, 29 (37), 11523-39 PMID: 19759300

How your emotional state affects how you hear speech

2009-09-17T11:21:00.009-04:00

I found an interesting study by Wang et. al investigating how the current emotional state that we find ourselves in modulates the auditory response of speech early in the sensory processing stream at the cortical level. Here's their abstract.

In order to understand how emotional state influences the listener's physiological response to speech, subjects looked at emotion-evoking pictures while 32-channel EEG evoked responses (ERPs) to an unchanging auditory stimulus (“danny”) were collected. The pictures were selected from the International Affective Picture System database. They were rated by participants and differed in valence (positive, negative, neutral), but not in dominance and arousal. Effects of viewing negative emotion pictures were seen as early as 20 msec (p = .006). An analysis of the global field power highlighted a time period of interest (30.4–129.0 msec) where the effects of emotion are likely to be the most robust. At the cortical level, the responses differed significantly depending on the valence ratings the subjects provided for the visual stimuli, which divided them into the high valence intensity group and the low valence intensity group. The high valence intensity group exhibited a clear divergent bivalent effect of emotion (ERPs at Cz during viewing neutral pictures subtracted from ERPs during viewing positive or negative pictures) in the time period of interest (rΦ = .534, p < .01). Moreover, group differences emerged in the pattern of global activation during this time period. Although both groups demonstrated a significant effect of emotion (ANOVA, p = .004 and .006, low valence intensity and high valence intensity, respectively), the high valence intensity group exhibited a much larger effect. Whereas the low valence intensity group exhibited its smaller effect predominantly in frontal areas, the larger effect in the high valence intensity group was found globally, especially in the left temporal areas, with the largest divergent bivalent effects (ANOVA, p < .00001) in high valence intensity subjects around the midline. Thus, divergent bivalent effects were observed between 30 and 130 msec, and were dependent on the subject's subjective state, whereas the effects at 20 msec were evident only for negative emotion, independent of the subject's behavioral responses. Taken together, it appears that emotion can affect auditory function early in the sensory processing stream.

Wang J, Nicol T, Skoe E, Sams M, & Kraus N (2009). Emotion modulates early auditory response to speech. Journal of cognitive neuroscience, 21 (11), 2121-8 PMID: 18855553

Coffee on the brain, spatial memory impairment, and how the immune system may help

2009-09-14T19:14:00.035-04:00

I'm constantly on the lookout for new research findings further substantiating sleep's significant effects on memory...perhaps in an attempt to finally convince myself that continuously misplacing my keys is NOT a normal part of young adulthood...and that 5 hours of shut-eye just isn't cutting it anymore (note to self: resist late night treks to Starbucks).

Coffee-drinking women on the other hand have an 18% lower chance of having visual and spatial memory declines according to a 2007 study by Ritchie et. al. "No relation was found between caffeine intake and cognitive decline in men"...NOT FAIR!

a link on How to Overcome a Starbucks Addiction

Anyway...a recent study by Girardeau et al. found online at Nature Neuroscience once again confirms sleep's important function on memory consolidation. They found that suppressing sharp wave-ripple (SPW-R) complexes in the hippocampus-entorhinal cortex of rats during post-training rest and sleep significantly impaired spatial memory. (I'd bet that we'd see similar effects by suppressing slow-wave sleep spindles in the thalamus as well).

The authors suggest that SPW-Rs play a crucial role in memory consolidation by temporarily compressing reactivations of waking firing sequences thus allowing activation of NMDA receptors and spike time-dependent plasticity.

You may be wondering at this point if there's anything you can do to avoid the risk of spatial memory loss other than getting good sleep. Well you're in luck. According to 2008 study conducted by Ron-Harel and colleagues functional cell-mediated immunity was necessary for the maintenance of hippocampus-dependent spatial memory in mice. In other words, the healthier the mice the better the spatial memory.

So remember kids, rest up and stay healthy or you might literally lose your marbles.

More about the origin of "losing your marbles" found here.

Ritchie, K., Carriere, I., de Mendonca, A., Portet, F., Dartigues, J., Rouaud, O., Barberger-Gateau, P., & Ancelin, M. (2007). The neuroprotective effects of caffeine: A prospective population study (the Three City Study) Neurology, 69 (6), 536-545 DOI: 10.1212/01.wnl.0000266670.35219.0c

Girardeau1,G, Benchenane1, K, Wiener, S I, Buzsáki G, & Zugaro1, M B. (2009). Selective suppression of hippocampal ripples impairs spatial memory.Nature Neuroscience : 10.1038/nn.2384

Ron-Harel N, Segev Y, Lewitus GM, Cardon M, Ziv Y, Netanely D, Jacob-Hirsch J, Amariglio N, Rechavi G, Domany E, & Schwartz M (2008). Age-dependent spatial memory loss can be partially restored by immune activation. Rejuvenation research, 11 (5), 903-13 PMID: 18803478

Destabilizing old memories with novel information

2009-09-12T12:51:00.025-04:00

What if one day we could disrupt unwanted consolidated memories like those of old traumatic experiences or even unforgettable heartbreaks and replace them with novel and more pleasant ones? Sounds like a tagline from the 2004 Oscar-winning film Eternal Sunshine of the Spotless Mind doesn't it?

Published in this month's issue of Learning & Memory, a study by Winters, Tucci, and DaCosta-Furtado over at the University of Guelph, Canada has managed to bring us one step closer to making this seemingly far-fetched idea a reality. They had rats explore sample objects and some time later injected them with either an NMDA receptor antagonist known as MK-801 or a control saline solution before reactivating the object memory.

The authors found that the reconsolidation of young or weakly encoded memories were disrupted by MK-801 regardless of the reactivation conditions. However, when they increased the amount of sample object exploration or the time between sample phase and reactivation (older and stronger memories) the effect of MK-801 was abolished during reconsolidation unless (now this is the interesting part) salient novel contextual information was present during memory reactivation. Their findings support the hypothesis that the reconsolidation process enables modification of existing memories.

Could this be a future treatment option for patients suffering from PTSD? How about for far less severe cases like those who just can't get over that one ex. For now it seems like we'll be seeing it "only in theaters".

Winters, B., Tucci, M., & DaCosta-Furtado, M. (2009). Older and stronger object memories are selectively destabilized by reactivation in the presence of new information Learning & Memory, 16 (9), 545-553 DOI: 10.1101/lm.1509909

Is inhibition a measure of free will?

2009-09-09T17:19:00.010-04:00

Reading Alwyn Scott's "Stairway to the Mind" I came across an interesting tidbit of information pointing out that human's have a greater percentage of inhibitory neurons compared to other animals (human 75% rabbit 31%). For some unknown reason this made me think about the tricky construct of free will and the question of whether free will could be better measured not by what we chose to do, but by what we chose not to do. In other words, could free will be measured by a capacity to inhibit certain thoughts and behaviors.

Upon further research I found Baer, Kaufman, and Baumeister's book "Are We Free? Psychology and Free Will". They also tossed around this question and came to an interesting conclusion. Here is a snippet from their work:

We have danced around the issue of whether conscious control is to be equated with free will; in fact, we suspect that at the most basic level, the answer is no...the ability to inhibit responses is powerful and one could reasonable make the argument that without it, free will would not be possible, because we would not be able to stop what some force (external or internal) seemed to impel us to do...If we do assume that free will can be directly observed in inhibition of behavior, then is free will measured by inhibition? The latter question is especially poignant with respect ot those people who show marked inhibition deficits, such as children, the elderly, and certain patient populations. If we agree with Libet (1999) and consider inhibition of an unconsciously determined action to be equivalent to free will, then these populations suffer from impaired free will...we see that this view is already implicitly, if not explicitly, accepted in many fields, as well as (to some degree) enshrined in common wisdom about behavior (Baer, Kaufman, & Baumeister 2008).

I reflect on Mischel, Shoda, and Rodriquez's well known 1989 experiment investigating delayed gratification in children and wonder whether those who decided to wait for the larger reward were not only "smarter", but had a greater capacity for free will as well. Can we associate intelligence with free will? What do you think?

Mischel, W., Shoda, Y., & Rodriguez, M. (1989). Delay of gratification in children Science, 244 (4907), 933-938 DOI: 10.1126/science.2658056

Baer, J., Kaufman, J. C., & Baumeister, R. F. (Eds.) (2008). Are we free? Psychology and free will. New York: Oxford University Press.

Scott, A. (1995). Stairway to the Mind: The controversial new science of consciousness. New York: Springer-Verlag.

Bullying boss disturbing your sleep?

2009-09-08T13:55:00.023-04:00

Its not uncommon that we're forced to work/put up with a disgruntled boss at one point or another. Not surprisingly, the relationship between an employee and their boss is the best predictor for job satisfaction according to a 2006 survey conducted by Accountemps, a Menlo Park, California-based specialized staffing service for temporary accounting, finance, and bookkeeping professionals. Moreover, the relationship you have with your boss may not only determine your overall job satisfaction, but also how well you sleep.

In a study by Niedhammer et. al published in the latest edition of SLEEP they investigated the association between a bullying boss and experienced sleep disturbance. Here is a snippet of their abstract:

Results: Workplace bullying was strongly associated with sleep disturbances. Past exposure to bullying also increased the risk for this outcome. The more frequent the exposure to bullying, the higher the risk of experiencing sleep disturbances. Observing someone else being bullied in the workplace was also associated with the outcome. Adjustment for covariates did not modify the results. Additional adjustment for self-reported health and depressive symptoms diminished the magnitude of the associations that remained significant.
Conclusions: The prevalence of workplace bullying (around 10%) was found to be high in this study as well was the impact of this major job-related stressor on sleep disturbances. Although no conclusion about causality could be drawn from this cross-sectional study, the findings suggest that the contribution of workplace bullying to the burden of sleep disturbances may be substantial.

This article ties in well with Levin and Nielsen's prior work on emotions and disturbed sleep. In their 2007 Psychological Bulletin paper they proposed that high affect load, the consequence of daily variations in emotional pressure, and high affect distress, the disposition to experience events with distressing, significantly influenced nightmare prevalence, frequency, severity, and psychopathological comorbidity.

I suspect the bullied employees who experience sleep disturbances are also experiencing an associated high affect load and high affect distress.

Niedhammer I; David S; Degioanni S; Drummond A; Philip P. Workplace bullying and sleep disturbances: findings from a large scale cross-sectional survey in the French working population. SLEEP 2009;32(9):1211-1219.

Niedhammer I, Chastang JF, & David S (2008). Importance of psychosocial work factors on general health outcomes in the national French SUMER survey. Occupational medicine (Oxford, England), 58 (1), 15-24 PMID: 17965447

Levin, R., & Nielsen, T. (2007). Disturbed dreaming, posttraumatic stress disorder, and affect distress: A review and neurocognitive model. Psychological Bulletin, 133 (3), 482-528 DOI: 10.1037/0033-2909.133.3.482

Erasing phobias early in life

2009-09-05T23:15:00.027-04:00

The model of fear extinction originated from the Pavlovian classical conditioning paradigm in the early 1900s. Defined as a reduction in a conditioned fear response following a non reinforced exposure to a feared conditioned stimulus, fear extinction is known to involve the amygdala and medial prefrontal cortex (mPFC).

It's also a frequently striven-for goal in cognitive behavioral therapy during the treatment of various phobias including arachibutyrophobia; the fear of peanut butter sticking to the roof of the mouth, or barophobia; the fear of gravity.

Unfortunately, extinguished fear responses sometimes reappear with the passage of time (spontaneous recovery), through a shift of context (renewal), or by unsignaled presentations of the unconditioned stimulus (reinstatement). However, the likelihood of these events happening after a few intense sessions of fear exposure may differ significantly depending on the age of the patient according to a new study published in this weeks Journal of Neuroscience.

Kim, Hamlin, and Richardson investigated the role of the mPFC during fear extinction among postnatal 24 day rats (P24) and postnatal 17 day rats (P17). They found that temporary inactivation of the mPFC during extinction training blocked extinction retention the following day in P24 rats but not in P17 rats.

Furthermore, through immunohistochemical analyses they observed that extinction of conditioned fear involved an increased number of phosphorylated MAPK-immunoreactive (pMAPK-IR) neurons in the mPFC and amygdala in P24 rats. However, an elevation of these neurons was only seen in the amygdala of P17 rats. The results indicate that the mPFC has no part in the neural circuitry underlying fear extinction in P17 rats.

The authors suggest that fear extinction is essentially the process of unlearning for the younger rats. In other words, they're "erasing" their fear altogether!

These important findings may significantly impact the future treatment of phobias; targeting and treating fears earlier rather than later in life. Perhaps one day we can teach little barophobic Johnny why the force of gravity isn't really such a scary thing after all.

Kim JH, Hamlin AS, & Richardson R (2009). Fear extinction across development: the involvement of the medial prefrontal cortex as assessed by temporary inactivation and immunohistochemistry. The Journal of neuroscience : the official journal of the Society for Neuroscience, 29 (35), 10802-8 PMID: 19726637

The neural correlates of lucid dreaming

2009-09-02T21:22:00.034-04:00

I've always had a deep fascination for lucid dreaming and only a handful of times have I been fortunate enough to experience such a wondrous and relatively rare state of consciousness. In one instance I decided to meditate and that blissful experience has no doubt left an indelible memory. So what's really going on in the brain during a lucid dream?

In a recent study Voss and colleagues over at Bonn University in collaboration with Hobson at Harvard Medical School decided to investigate the electrophysiological correlates of lucid dreaming. They attempted to train 20 undergraduate students in the art of lucid dreaming via pre-sleep autosuggestions over a four month period and were able to successfully train 6. These subjects then spent a few nights at a sleep lab hooked up to an EEG machine. Only half were able to experience lucid dreaming during their stay(now you can see how tough it actually is to induce a lucid dream).

You may be wondering at this point how the researchers know subjects are in a lucid dreaming state. Apparently subjects can be trained to make voluntary horizontal eye movements during sleep indicating lucidity.

The authors found that during lucid dreaming there was a shift in EEG power, especially in the 40hz range and in the frontal regions of the brain. They suggest that this change in brain physiology is somehow associated with the lucid dreamer's ability to self-reflect and gain volitional control; activities absent in regular REM dreaming. They conclude that lucid dreaming involves features of both REM sleep and waking, categorizing it as a "hybrid state" and hypothesize that "lucidity arises when wake-like frontal lobe activation is associated with REM-like activity in posterior structures".

I can't help but wonder what the different factors are that make certain individuals adept at lucid dreaming. And just imagine the endless possibilities if we were only able to figure out a sure-fire way to lucid dream on command. Perhaps an artistic outlet, a method of coping, a form of therapy? Maybe I'm just dreaming.

I provide a wikihow link on how to lucid dream. I'm not sure how well it'll work but try it out for yourself and remember...don't be afraid to dream big.

Open access to the full article is available here.
Thanks superkuh!

Voss U, Holzmann R, Tuin I, & J A Hobson (2009). Lucid Dreaming: A State of Consciousness with Features of Both Waking and Non-Lucid Dreaming Sleep, 32 (9), 1191-1200 Other: 27567

Hobson, J. (2005). Sleep is of the brain, by the brain and for the brain Nature, 437 (7063), 1254-1256 DOI: 10.1038/nature04283

The peripheral attenton deficit of primary psychopaths

2009-08-31T16:40:00.034-04:00

Described as cold, heartless, manipulative, selfish, and low anxiety, primary psychopaths frankly scare the bejesus out of most people including myself. Look at the case of John Wayne Gacy Jr., the American serial killer who took the lives of 33 boys and young men between 1972 to 1978; burying most of the bodies in his crawl space beneath his home. During his sentencing he was quoted to have morbidly joked that the only thing he was guilty of was "running a cemetery without a license". How messed up is that?

Even until the day of his execution, Gacy never expressed any remorse for the atrocities he had committed. Interestingly enough, the lethal chemicals contained in the IV tube leading to his arm unexpectedly solidified, prolonging the execution process. I can't help but believe that on that day karma came back and bit him in the ass...hard (I just wanted to make it clear that I'm not saying all psychopaths are serial killers).

So what were the reasons that led the truly disturbed Gacy to hone in on performing these heinous acts while ignoring all the circumstances that may have inhibited him from following through? One possible explanation known as the response modulation hypothesis purports that primary psychopaths are relatively insensitive to contextual information, that this neglect undermines their responsiveness to environmental information that normally facilitate self-regulation, and that they have an attentionally mediated deficit reducing processing of inhibitory cues outside the focus of attention (i.e. Gacy couldn't attend to all the peripheral information telling him not to murder his victims).

Zeier, Maxwell, and Newman over at the University of Wisconsin-Madison decided to test this hypothesis by having 110 incarcerated men perform on a modified version of the flanker task which tests the role of attention in the moderation of response to inhibitory information. Results showed that primary psychopaths were significantly less affected by peripheral response-incongruent information compared to a control group confirming the response modulation hypothesis.

The study demonstrates that attention plays a crucial role in moderating sensitivity to contextual information in primary psychopaths. However, the authors note that their findings do not necessarily apply to secondary (i.e. high-anxious) psychopathic subtypes and that their experiment did not manipulate motivational and emotional factors. They conclude by stating that their findings represent an important next step toward further understanding and treating psychopathy.

Reading this article led me to ponder over a few provocative questions of my own. Does it ultimately make Gacy a victim of his own peripheral attention deficit? Should he have been held 100% accountable for his actions due to seemingly faulty brain wiring? Was he given a fair shake in court when his plea of insanity was outright rejected? What about other primary psychopaths who've committed considerably less severe crimes? I suppose that's for you to decide.

Zeier JD, Maxwell JS, & Newman JP (2009). Attention moderates the processing of inhibitory information in primary psychopathy. Journal of abnormal psychology, 118 (3), 554-63 PMID: 19685952

The association between creativity and suicide

2009-08-29T01:50:00.041-04:00

Over the years a number of iconic musicians have met tragic deaths from either an overdose or suicide (e.g. Bradley Nowell and Kurt Cobain from two of my favorite bands); the former a possible mode of the latter.

In light of DJ AM's recent passing, a prescription drug overdose the most likely culprit, and today's commemoration of Michael Jackson's 51st birthday, I couldn't help but ponder the possible associations between creativity, psychopathology, and suicide. Where is that fine line between creative genius and psychopathology? Does it take a severe mood disturbance to produce a truly creative work of art...to the point of self-destruction? Are musicians more vulnerable to psychopathology and at higher risk for attempting suicide? I provide a few abstracts from past studies addressing this fascinating topic.

Virginia Woolf as an example of a mental disorder and artistic creativity
This is an attempt to evaluate the mental disorder that the novelist Virginia Woolf suffered, and to determine the relationship between her creativity and her insanity. What mostly characterizes her illness is the presence of typical phases of severely impairing depression and significant hypomania, culminating in suicide at the age of 59. This is a convincing life history of a bipolar II disorder, although the "broad bipolar spectrum" is less easy to define operational than bipolar disorder I. She was moderately stable as well as exceptionally productive from 1915 until she committed suicide in 1941. Virginia Woolf created little or nothing while she was unwell, and was productive between attacks. A detailed analysis of her own creativity over the years shows that her illnesses were the source of material for her novels.

Musical creativity and suicide
The different abilities involved in artistic creativity may be mirrored by differences among mental disorders prevalent in each artistic profession, taking poets, painters, and composers as examples. Using suicide rates as a proxy for the prevalence of mental disorders in groups of artists, we investigated the percentage of deaths by suicide in a sample of 4,564 eminent artists who died in the 19th and 20th centuries. Of the sample, 2,259 were primarily involved in activities of a linguistic nature, e.g., poets and writers; 834 were primarily visual artists, such as painters and sculptors; and 1,471 were musicians (composers and instrumentalists). There were 63 suicides in the sample (1.3% of total deaths). Musicians as a group had lower suicide rates than literary and visual artists. Beyond socioeconomic reasons, which might favour interpretations based on effects of health selection, the lower rate of suicides among musicians may reflect some protective effect arising from music.

Suicide among eminent artists
To evaluate suicide risk by profession among eminent artists data from Garzanti's Encyclopedia, a broad biographical repertory, were used. Six categories in the visual and literary arts were compared: architects, painters, sculptors, writers, poets, and playwrights. Only people whose deaths occurred in the 1800s or 1900s were included since it is likely that underestimation of suicide has been lower in the more recent centuries. A total of 59 suicides were observed in a sample of 3,093 people: this corresponds to a ratio of 1.90%. Suicides were 51 among men (ratio 1.75%) and 8 among women (ratio 4.30%). The comparison by profession indicates that poets and writers exceed the mean suicide ratio of the sample. Painters and architects, conversely, have a clearly lower risk than the mean. Mean age of suicides was 44 yr. (SD = 12), with writers being slightly older (48 yr., SD = 12) than other artists. Artists who died of causes other than suicide reach a mean of 65 yr. (SD = 10). Suicide among artists seems to have a peculiar pattern, clearly different from the pattern of the general population, wherein suicide risk is higher among men and older people. Adverse financial circumstances and the stress attributed to rejection of personal products may contribute to the specific risk of suicide among artists. The link between mental disorders, such as manic-depression, which imply a higher risk of suicide, and creativeness is discussed as a contributing factor.

Gender and suicide risk among artists: a multivariate analysis
Research on mental disorders among male artists has suggested that artists are at risk of suicide. However, given that men are higher in suicide risk than women, the presumed suicide risk of artists may be an artifact of sampling bias. A logistic regression analysis of data from 21 states finds that artists have 270% higher risk of suicide than nonartists. However, after controlling for gender and sociodemographic variables, this risk level is reduced to 125%. The findings are related to both psychiatric and work-related stress factors that may place artists at risk of suicide as an occupational group.

Creativity, depression and suicide
The relationship between suicide and creativity has long been a subject of considerable concern. The author presents evidence indicating that in fact depression, suicide, and creativity are related. Several hypotheses for the relationship are posited. It is suggested that the same changes in the serotonergic system that are associated with depression in general and with impulsive suicides and homicides in the extreme may also be responsible for an element of risk taking that characterizes creativity and innovation in a person psychodynamically predisposed to being creative.

The relation between depression and art
The relationships between depression and art are many and varied. Examples of poets, novelists, and musicians spring to mind who have vividly portrayed depression, usually from personal experience of it. These portrayals often had a psychohygienic significance for the artists concerned--as in the case of Goethe, who, in writing 'The sorrows of young Werther', exorcised his own suicidal impulses and thoughts, thus probably saving his own life. Artists have also depicted the physiognomy of depressives, e.g. Hans Baldung Grien in his picture 'Saturn' showing the pronounced nasolabial folds described by Veraguth as indicative of melancholia. Relationships between depression and art also play a role in certain theories of creativity, such as that of Silverman, who postulates that in the depressive phase new impressions arise which then find their expression in a manic phase. Finally, there are the various creative therapies designed in cases of depression (e.g. by encouraging the patient to paint or draw) to reactivate the nondominant hemisphere of the brain. Particularly in chronic or recurrent depressions this reactivation also serves to open up to the patient new perspectives for the solution of the problems that drive him into depression.

In response to Devin's question about a conclusion I write:

"Ah yes...the conclusion...seems like the use of a diathesis-stress model would be appropriate to explain a few of the overdoses and suicides among the creative. Lots of artists tend to derive their inspiration from the lowest of lows and the highest of highs. It's also not highly unusual that they're constantly surrounded by an environment that condones the use of various drugs...especially if they make it big.

I suppose a preliminary model could look like this:

predisposition for creative abilities and mood disorder -> development of creative abilities along with adverse life events growing up-> drug addiction -> fame -> added stress -> major adverse life event -> overdose -> death

It all seems to come down to level of resiliency."

"Last days...in part, fictional." - Kurt Cobain

Popular musicians who committed suicide

Notable people who died from drug-related causes

Figueroa C G (2005). [Virginia Woolf as an example of a mental disorder and artistic creativity] Revista medica de Chile, 133 (11), 1381-8 PMID: 16446863

Preti A, De Biasi F, & Miotto P (2001). Musical creativity and suicide. Psychological reports, 89 (3), 719-27 PMID: 11824743

Preti A, & Miotto P (1999). Suicide among eminent artists. Psychological reports, 84 (1), 291-301 PMID: 10203964

Stack S (1996). Gender and suicide risk among artists: a multivariate analysis. Suicide & life-threatening behavior, 26 (4), 374-9 PMID: 9014267

Slaby AE (1992). Creativity, depression and suicide. Suicide & life-threatening behavior, 22 (2), 157-66 PMID: 1626330

Pöldinger W (1986). The relation between depression and art. Psychopathology, 19 Suppl 2, 263-8 PMID: 3575627

The search for a quantum psychology

2009-08-28T15:46:00.012-04:00

Today I provide you with a few links to information on "quantum psychology" and the various ways people are attempting to integrate the two sciences.

Robert Anton Wilson
http://www.rawilson.com/quantum.html

The Quantum Psychology Project
http://www.quantumpsychology.com/index-e.html

Physical Foundations of Quantum Psychology
http://htpprints.yorku.ca/archive/00000289/

Mass Density Blog
http://www.massdensity.com/

Yet another reason not to consume cannabis

2009-08-27T14:09:00.017-04:00

In 1936 an exploitation film directed by Louis Gasnier called Reefer Madness was made in an attempt to teach parents about the dangers of cannabis use. It told of fictional highschool students experimenting with the drug and their tragic and utterly ridiculous demise (e.g. manslaughter, rape, suicide). I'm pretty sure the majority of us now know that smoking marijuana will not cause someone to go on a murderous rampage or off themselves just because they're high. However, recent studies have found that cannabis use does have some negative effects on long-term memory.

Puighermanal and her colleagues investigated the possible involvement of the mTOR pathway in the cognitive impairments produced by cannabinoid agonists. mTOR is a type of enzyme that regulates multiple cellular processes such as neural development and long-term modification of synaptic strength. Administering acute amounts of THC (3 or 10 mg per body weight) to mice, they found modulation of the mTOR/p70S6K signaling cascade in the hippocampus and measurable deficits in long-term memory on an object and context recognition test. However, lower doses did not produce any significant effects.

The authors explain that CB1R activation by exogenous or endogenous cannabinoids can trigger the activation of the mTOR pathway and protein synthesis in the hippocampus through a glutamatergic mechanism which underly the long-term memory impairment. They conclude by pointing out the serious drawbacks of cannabis consumption (i.e. amnesic effects) and believe that their findings would be useful for the development of new therapeutic strategies leading to the prevention of negative side effects of cannabis use. C'mon guys, lets get crackin'!

The film ends with the ominous warning "TELL YOUR CHILDREN" in large text. Yes friends, tell your children...that is...if you can remember to. ::cues overly dramatic music::

Puighermanal, E., Marsicano, G., Busquets-Garcia, A., Lutz, B., Maldonado, R., & Ozaita, A. (2009). Cannabinoid modulation of hippocampal long-term memory is mediated by mTOR signaling Nature Neuroscience, 12 (9), 1152-1158 DOI: 10.1038/nn.2369

Remote Memories finally released from the diabolical grip of Hippocampus

2009-08-26T02:16:00.026-04:00

Hippocampus is suspect in its involvement with the evil legion of brain tissue infamously known as The Retrieval Network, relentlessly capturing Recent Memories. A wise oracle, The System-Level Consolidation Model, foretells the transformation of Recent Memories into Remote Memories and their eventual release from the inexorable grip of Hippocampus as they change hands to the sluggish yet more powerful Neocortical Circuitry during a dark and tortuous time known as the Period of Consolidation (if you haven't gotten it yet, I've been attempting to maintain a consistent theme with the ridiculous title of this blog entry...funny what sleep deprivation and 20 odd years of dorkdum will do to a person).

All kidding aside, Takashima et al. at Radboud University Nijmegen of the Netherlands conducted a study testing the standard system-level consoldiation model's hypothesis. They measured brain activity and connectivity during retrieval of face-location associations using an fMRI. Face-location associations were used for three reasons; features of this stimuli lead to distinct neocortical activity in the fusiform gyrus and posterior parietal cortex, binding of between-domain association involves the hippocampus, and a cued-recall paradigm elicits activation of the hippocampus. Two delays were used; 15 minutes and 24 hours including a whole night of sleep.

Consistent with the their hypothesis and the standard model, results showed that posterior hippocampal activity associated with high-confidence retrieval decreased while neocortical activity increased with a 24 hour period of consolidation. Moreover, they found that connectivity between the hippocampus and neocortical regions decreased as cortical-cortical connectivity between the representational areas increased.

This study supports a two-level process of the declarative memory system. The authors infer from the present and previous studies that the hippocampus is more likely suited for rapid encoding and retention of information by linking neocortical representations. However, the hippocampus seems to be an unlikely repository for long-term memory.

Sorry to break it to you Hippocampus, but the secret's out...you aren't as powerful as once thought to be ::end of anthropomorphism::.

Takashima, A., Nieuwenhuis, I., Jensen, O., Talamini, L., Rijpkema, M., & Fernandez, G. (2009). Shift from Hippocampal to Neocortical Centered Retrieval Network with Consolidation Journal of Neuroscience, 29 (32), 10087-10093 DOI: 10.1523/JNEUROSCI.0799-09.2009

An overnight therapy session...without a therapist

2009-08-25T14:05:00.009-04:00

Today I point you toward a fascinating review article by Walker and van der Helm looking at the crucial function of sleep on emotional regulation. Here is a snippet of their abstract:

This review surveys an array of diverse findings across basic and clinical research domains, resulting in a convergent view of sleep-dependent emotional brain processing. On the basis of the unique neurobiology of sleep, the authors outline a model describing the overnight modulation of affective neural systems and the (re)processing of recent emotional experiences, both of which appear to redress the appropriate next-day reactivity of limbic and associated autonomic networks. Furthermore, a rapid eye movement (REM) sleep hypothesis of emotional-memory processing is proposed, the implications of which may provide brain-based insights into the association between sleep abnormalities and the initiation and maintenance of mood disturbances.

Sleep FTW!

Walker, M., & van der Helm, E. (2009). Overnight therapy? The role of sleep in emotional brain processing. Psychological Bulletin, 135 (5), 731-748 DOI: 10.1037/a0016570

Bid farewell to sleep deprivation's adverse effects on memory

2009-08-24T16:17:00.018-04:00

Graveyard shifts and all-night cram sessions are probably some of the worst things you can do to your brain and body. I know because sadly I've done both more times than I can count. It is well known in the sleep field that chronic sleep deprivation accelerates the adverse effects of aging (damn these premature wrinkles), causes emotional dysregulation, and significantly impairs memory.

However, Chua et al. over at the Duke-NUS Graduate Medical School in Singapore seem to have discovered a miracle drug that helps sleep-deprived individuals protect episodic memory; memory consisting of autobiographical events such as times, places, and associated emotions. They found that Donepezil, a cholinesterase inhibitor, reduced episodic memory impairment in 24 hour sleep-deprived healthy young subjects.

The authors suggest that Donepezil works by improving attention as well as enhancing memory encoding in sleep-deprived individuals only (subjects received no benefit from the drug when they were well rested). Future studies should further investigate Donepezil and other cholinesterase inhibitors' effects on memory functioning of Alzheimer's disease patients as many of them seem to have comorbid sleep disorders.

Remember Adderall, the popular psychostimulant procrastinating college students use to take during all-nighters? Could Donepezil become the new and improved fad? Only time will tell...

Chuah LY, Chong DL, Chen AK, Rekshan WR, Jian JC, Zheng H, & Chee MW (2009).Donepezil improves episodic memory in young individuals vulnerable to the effects of sleep deprivation. SLEEP, 32, 999-1010.

Chuah LY, & Chee MW (2008). Cholinergic augmentation modulates visual task performance in sleep-deprived young adults. The Journal of neuroscience : the official journal of the Society for Neuroscience, 28 (44), 11369-77 PMID: 18971479

Tone deaf? blame it on poor connectivity

2009-08-21T01:29:00.021-04:00

Tone deafness is defined as the inability to discriminate between musical notes also known as amusia, tune deafness, dysmelodia, and dysmusia. Famous leaders including President Theodore Roosevelt and Ernesto "Che" Guevara have suffered from this often embarrassing hearing impairment. In an epic fail, Che once tried to woo some chicas at a dance by performing a tango while the band was playing a lively Brazilian (sigh). These are the kinds of people you would never bring to a karaoke bar...unless, of course you were tone deaf too. In that case it wouldn't really matter now would it?

Loui, Alsop, and Shlaug from Beth Israel Deaconess Medical Center and Harvard Medical School further investigated tone deafness and its association with the arcuate fasciculus (AF), a fiber tract connecting temporal and frontal brain regions. Using diffusion tensor tractography combined with perception and production psychophysics, they found that tone deaf subjects had a lack of neural connectivity in the AF compared to a control group. They seemed to possess fewer fibers in this particular area of the brain with at least one of the superior AF branches being unidentified by imaging parameters.

The authors demonstrate for the first time that the AF is a neural correlate of auditory-motor behavior where AF volume can be an effective predictor of vocal behavior. They suggest that tone deafness should be considered a new disconnection syndrome resulting in impaired pitch perception and vocal sound production.

The next time you find yourself at a karaoke bar with your good buddies Theo and Che, before punching in that code for the latest Kris Allen song, double check to make sure you've got good connection.

Loui, P., Alsop, D., & Schlaug, G. (2009). Tone Deafness: A New Disconnection Syndrome? Journal of Neuroscience, 29 (33), 10215-10220 DOI: 10.1523/JNEUROSCI.1701-09.2009

Did sleepwalking once serve as an adaptive function?

2009-08-20T14:26:00.035-04:00

I readily admit that I use to sleepwalk as a kid. My dad once found me laid out at the foot of our considerably large staircase completely unscathed! As I reflect back on those sometimes hazardous, but mostly humorous unconscious experiences I can't help but wonder if somnambulism, the formal term for sleepwalking, once served as some kind of adaptive function. Were our ancient ancestors afforded the opportunity to escape the perils of the wild during states of deep sleep?

There are countless stories of somnambulists executing complex escape behaviors, performing extraordinary feats, and seriously harming others. In 1987 Kenneth Parks drove 15 miles to his in-law's home, beat his father-in-law until he was unconscious, and stabbed his mother-in-law to death...doing all of this while asleep. He later went to the police station stating, "I think I have killed some people". He was covered in blood with a badly injured hand and had absolutely no recollection of what he had done. A year later he was acquitted of murder. Apparently one can get away with a lot on the basis of automatism; even the heinous crime of rape according to Ebrahim at the London Sleep Centre.

So why do people sleepwalk? Researchers like Pilon, Montplaisir, and Zadra have shown that probable causes of somnambulism can be due to a variety of factors such as stress, anxiety, sleep deprivation, or an external disturbance. Parks was unemployed, a gambaholic, and highly stressed. However, this doesn't really answer my original question. Was there an evolutionary purpose to this seemingly useless and bizarre phenomena or is it merely the behavioral manifestation of a sleep disorder?

Mahowald and Schenck at the Minnesota Regional Sleep Disorder Center seem to believe that somnambulism is a form of threat simulation gone awry during NREM sleep. This explanation suggests that there is, in part, an evolutionary role to the curious phenomena under consideration, but some kind of malfunctioning has taken place that doesn't serve any added purpose.

What if we were to look toward our primate brethren for the answer? Do apes and chimpanzees experience sleepwalking too? Kantha at Kyoto University conducted a literature review on somnambulism in non-human primates and found absolutely no evidence for this. However, she adds that it may be due to limitations in expertise and methodological resources.

For now it seems that somnambulism is found exclusively in humans and may have been a fairly recent phenomena set off by the ill's of modern man. I suppose if you're still curious about this fascinating subject you can conduct your own little personal experiment. The next time you witness a hunger repressed friend or loved one sleepwalking towards the fridge for a late night snack...try wrestling them to the ground and observe what happens.

Ebrahim IO (2006). Somnambulistic sexual behaviour (sexsomnia). Journal of clinical forensic medicine, 13 (4), 219-24 PMID: 16564199

Kantha SS (2003). Is somnambulism a distinct disorder of humans and not seen in non-human primates? Medical hypotheses, 61 (5-6), 517-8 PMID: 14592779

Mahowald MW, Schenck CH, Rosen GM, & Hurwitz TD (1992). The role of a sleep disorder center in evaluating sleep violence. Archives of neurology, 49 (6), 604-7 PMID: 1596195

Pilon M, Montplaisir J, & Zadra A (2008). Precipitating factors of somnambulism: impact of sleep deprivation and forced arousals. Neurology, 70 (24), 2284-90 PMID: 18463368

The consequences of repetitive thought, thought, thought...

2009-08-19T12:15:00.007-04:00

I recently stumbled upon an interesting review by Watkins on the constructive and unconstructive consequences of repetitive thought (RT). He mentions a number of thought processes involved in this concept refined by Segerstrom in 2003 including rumination, worry, perseverative cognition, cognitive and emotional processing, counterfactual thinking, mind wandering, defensive pessimism, and habitual negative self-thinking.

His review of the research literature reveals that the main constructive consequences of RT are recovery from trauma and the ability to plan ahead while the unconstructive consequences are depression and anxiety. Three main factors seem to determine the consequences of your RT; the valence or emotional value of the thought content, the interpersonal and situational context in which you are in while having the RT, and the construal level or perception of the RT.

And here I thought RT was always a bad thing...

You can find the full text here.

Watkins ER (2008). Constructive and unconstructive repetitive thought. Psychological bulletin, 134 (2), 163-206 PMID: 18298268

Androgen's effects on older female cognitive functioning

2009-08-18T12:25:00.013-04:00

Nowadays there seems to be a growing concern for age-related cognitive decline evidenced by the countless number of ads promising brain enhancement through the guise of drugs and nutrients. In addition, studies have shown that female mice exhibit more severe cognitive decline compared to age-matched male mice. So does this mean women should be more vigilant of their brain health and head for the pharmacies before it's too late? Or is all this hoopla just smoke and mirrors?

A recent study conducted by Benice and Raber over at the Oregon Health & Science University may provide us with more information to better answer these questions. Their primary aim was to see whether androgen levels affected spatial memory. They tested 22-24 month old female mice treated for 6 weeks with either testosterone, dehyrdrotestosterone, or placebo capsules. Female mice treated with testosterone showed enhanced performance in a water maze measuring spatial memory retention compared to female mice treated with a placebo. In contrast, female mice treated with dehydrotestosterone showed improvement in passive avoidance retention.

The results of this study provide evidence that androgen supplementation improves cognitive performance in older female mice depending on the cognitive task and type of hormone treatment. Now all we need to know is whether these findings translate to humans.

Benice TS, & Raber J (2009). Testosterone and dihydrotestosterone differentially improve cognition in aged female mice. Learning & memory (Cold Spring Harbor, N.Y.), 16 (8), 479-85 PMID: 19633137

Autobiographical and nonautobiographical memory functioning in PTSD

2009-08-15T14:18:00.014-04:00

Posttraumatic stress disorder (PTSD) is a debilitating disorder characterized by altered memory functioning including the unintentional reliving of the traumatic experience. This feature of the disorder has been the focus of most PTSD studies, however rarely has there been an investigation on the aspect of disturbed intentional recall within the PTSD patient population.

Jelinek et al. decided to address the paucity in this area of research by first clarifying central qualitative and quantitative aspects of memory functioning in PTSD and then combining prior research on autobiographical and nonautobiographical memory to examine whether memory disorganization of the traumatic event exceeded impairment of verbal memory.

Subjects consisted of 81 adult victims of single traumatic events and 30 nontraumatized controls. They were asked to partake in short interviews, give detailed reports traumatic and nontraumatic events, and complete a task that measured content and sequence memory performance.

Results showed that memories of the trauma were more disorganized than memories of an unpleasant control event in subjects with PTSD compared to subjects without PTSD. Significant group differences remained even after controlling for several confounding variables such as verbal intelligence. However, there were no significant differences in nonautobiographical performance between both groups and no evidence that organization of nonautobiographical memory was impaired in PTSD. This seems to make sense seeing as different brain structures are involved in both types of memory.

The authors note a couple of limitations including the use of only one nontraumatic control event and the introduction of a systematic time difference between the autobiographical control event and the trauma. They conclude by suggesting the use of neuroimaging techniques in future studies involving the disorganization of memory.

Jelinek L, Randjbar S, Seifert D, Kellner M, & Moritz S (2009). The organization of autobiographical and nonautobiographical memory in posttraumatic stress disorder (PTSD). Journal of abnormal psychology, 118 (2), 288-98 PMID: 19413404

Implicit-memory involved in accurate responding on recognition test

2009-08-14T14:28:00.013-04:00

There is a common assumption that accurate recognition exclusively reflects explicit-memory processing. However, Voss and Paller seem to have turned this notion on its head. In their study they found that implicit-memory processes can in fact guide responses in an explicit recognition test.

Kaleidoscope images were used to either divide or keep intact the human subject's attention. These same images were then discriminated from visually similar foils during forced-choice recognition testing.

They found higher accuracy for images studied with divided attention than for images studied with no attentional diversion. Surprisingly, "guess" responses were even more accurate than "know" responses. Moreover, metamemory was disrupted during the divided attention condition. ERPs of 200-400ms were observed for correct guesses which have been attributed to implicit-memory processing in past studies.

The authors suggest that implicit-memory processing to recognition may have been enhanced due to reduced potential for explicit-memory processing. They conclude by stating that their study "provides an unprecedented demonstration of the distinctive nature of overt recognition derived from unconscious memory, a phenomena that we describe as ‘implicit recognition.’"

Voss JL, & Paller KA (2009). An electrophysiological signature of unconscious recognition memory. Nature neuroscience, 12 (3), 349-55 PMID: 19198606

Do adults with Asperger syndrome really have ToM?

2009-08-14T00:51:00.024-04:00

People with autism are known to lack the ability to automatically attribute mental states to self and others also known as "mindblindness". A result of this impairment is failure on verbally instructed false-belief tasks.

However, people with Asperger syndrome, a milder form of autism, seem to pass with flying colors. This presents a problem for the "mindblindness" theory. Do people with Asperger syndrome really have a theory of mind (ToM) contrary to popular theory?

Senju, Southgate, White, and Frith decided to take it upon themselves to sort out this confusion. Instead of using verbal instructions, they had adults with Asperger syndrome perform an eye-tracking task that measured the spontaneous ability to mentalize. This entailed subjects viewing a scene of an actor first placing a ball into one of two boxes, then having a puppet move the ball to the alternative box unbeknownst to the distracted actor, thus causing a false belief in the actor about the location of the ball.

Results showed that the Asperger group had significantly less looking bias toward the correct window compared to a control group indicating the Asperger group's inability to spontaneously anticipate others' actions in a nonverbal task. It seems that to a certain extent they do lack a ToM. But then how are they able to pass the verbally instructed false-belief task? The authors suggest that because they are higher functioning compensatory learning is involved.

Senju A, Southgate V, White S, & Frith U (2009). Mindblind Eyes: An Absence of Spontaneous Theory of Mind in Asperger Syndrome. Science (New York, N.Y.) PMID: 19608858

Early-exposure to a high fat diet shapes future preference

2009-08-13T13:08:00.023-04:00

It goes without saying that the US is currently experiencing a rapidly growing obesity epidemic. Researchers from various fields continue to look for possible causes and solutions to such a deleterious medical condition. A recent study conducted by Teegarden, Scott, and Bale seem to have advanced our understanding of obesity just a bit further.

In a 10 day macronutrient choice preference test they found that high fat diet early-exposed mice exhibited a significantly greater preference for a high fat diet later on as adults measured by daily caloric intake. As a control for diet familiarity, mice exposed to a high carbohydrate diet during early life showed no differences in adult macronutrient preferences.

Interestingly, although there was increased proportional intake of the high fat diet within the early-exposed mice, there were no differences in total caloric intake or weight gain during the macronutrient choice preference period compared to a control group. This suggests that exposure seems to impact preference only.

The authors explain that the early-exposed mice exhibited significant changes in biochemical markers of dopamine signaling in the nucleus accumbens which altered long-term programming of mechanisms important in dietary preferences and reward.

This study makes me think of the countless number of youths I've see chowing down at McDonalds (I was one of them). It's unfortunate that the parents aren't able to see the bleak distant future of their children; lined up at a drive-through eagerly awaiting that first bite of the savory double cheeseburger and one step closer to developing heart disease.

Teegarden SL, Scott AN, & Bale TL (2009). Early life exposure to a high fat diet promotes long-term changes in dietary preferences and central reward signaling. Neuroscience, 162 (4), 924-32 PMID: 19465087

The relationship between a leftward bias and negative emotional recognition

2009-08-12T14:38:00.013-04:00

There appears to be a growing body of evidence supporting the relationship between space and emotion. For example, a fascinating study by Tamagni, Mantei, and Brugger found that healthy right handed subjects who exhibited a leftward line bisection bias on a lateralized lexical decision task had a recognition advantage for negative over positive emotional words.

The authors suggest that functional hemispheric differences state variables may be less decisive than the trait variable of lateral hemispatial attention and propose a reconsideration of "hemisphericity". Their findings also have complex implications for the interaction between cortical (anterior and posterior)and subcortical structures in the mediation of both the production of emotions and perception.

Tamagni C, Mantei T, & Brugger P (2009). Emotion and space: lateralized emotional word detection depends on line bisection bias. Neuroscience, 162 (4), 1101-5 PMID: 19501133

The power of imagination on prejudice

2009-08-11T14:54:00.017-04:00

Contact theory seems to be the new hot topic when it comes to solving the age old problem of prejudice. The theory simply states that given the right conditions if members of differing groups come in contact with one another, the interaction ultimately leads to more positive intergroup relations.

Crisp and Turner decided to pose a fascinating question. What if members of those groups didn't actually meet, but simply imagined the positive social interaction? Would the results still be significant? Research has shown that imagining a social situation can have the same effect as the real thing so Crisp and Turner weren't too far off the mark when they decided to persue this line of inquiry.

Reviewing the research, indeed they found that imagined contact improved intergroup attitudes, greater projection of positive traits to outgroups, reduced anxiety, and reduced stereotype threat. Some examples they included were the changing of young people's attitudes toward older people, straight men's attitudes toward gay men, and Mexican people's attitudes toward Metizos in Mexico. They were able to rule out cogntive load, demand characterstics, stereotype priming, and positive affect as possible alternative explanations.

One limitation of imagined contact that the authors mention is its weaker impact compared to more direct forms of intergroup contact. Another limitation I can think of is the daunting task of getting people to actually practice this new form of exposure, but first they must be willing to challenge their preconceived notions rather than continue to follow an "ignorance is bliss" philosophy.

Crisp, R., & Turner, R. (2009). Can imagined interactions produce positive perceptions?: Reducing prejudice through simulated social contact. American Psychologist, 64 (4), 231-240 DOI: 10.1037/a0014718

The negative health effects of perceived discrimination

2009-08-10T12:34:00.014-04:00

Discrimination has undoubtedly been the cause of suffering for many throughout human history. There have been countless reviews investigating the effects of discrimination on health, but none that have quite looked at the quantitative nature of this relationship. Pascoe and Richman decided to undertake this task by examining the strength of the evidence for the effect of perceived discrimination on multiple health outcomes through a meta-analysis.

The researchers discovered that an increased level of perceived discrimination is associated with more negative mental and physical health. In addition, they found that perceived discrimination was associated with heightened psychological and physical stress responses as well as increased participation in unhealthy behaviors. These relationships remained even when important covariates such as demographics were analyzed. Moderating variables included social support and coping style.

So the next time you feel like you're being unfairly discriminated against be sure to have lots of family and friends to back you up, think logically through the problem, and take action!

Pascoe EA, & Smart Richman L (2009). Perceived discrimination and health: a meta-analytic review. Psychological bulletin, 135 (4), 531-54 PMID: 19586161