Video at the speed of light.

The N.Y. Times points to extraordinary work that captures the image of a light pulse moving through an object, vastly faster than previous high speed photography. The technique might replace current ultrasound imaging in medical technology with photon imaging.

Taming human conflicts in the real world

Alexander and Christia provide a social psychology experiment that doesn't use Western undergraduate psychology students as subjects! They were provided the opportunity by a natural experiment that resulted from the consolidation of four Mostar high schools into three, yielding corat-majority, bosniac-majority and heterogeneous ethnic compositions. The students participated in economic experiments that pit an individual's self interest against the welfare of other participants. These others sometimes belong to the same ethnic group, and sometimes not, at integrated as well as segregated schools. This allowed the authors to measure the willingness to cooperate with others:

Whereas altruism drives the evolution of human cooperation, ethno-religious diversity has been considered to obstruct it, leading to poverty, corruption, and war. We argue that current research has failed to properly account for the institutional environment and how it affects the role diversity plays. The emergence of thriving, diverse communities throughout human history suggests that diversity does not always lead to cooperation breakdown. We conducted experiments in Mostar, Bosnia-Herzegovina with Catholic Croats and Muslim Bosniaks at a critical historic moment in the city’s postwar history. Using a public goods game, we found that the ability to sanction is key to achieving cooperation in ethno-religiously diverse groups, but that sanctions succeed only in integrated institutional environments and fail in segregated ones. Hence, we show experimentally for the first time in a real-life setting that institutions of integration can unleash human altruism and restore cooperation in the presence of diversity.

Our biological immune system activates our behavioral immune system.

Viewing disease cues (skin lesions, someone sneezing) leads people to display a heightened biological immune response (for example, stimulated production of cytokine interleukin-6). Miller and Maner now provide evidence for the converse: Activation of the biological immune system promotes activation of the behavioral immune system. Their abstract:

Activation of the behavioral immune system has been shown to promote activation of the biological immune system. The current research tested the hypothesis that activation of the biological immune system (as a result of recent illness) promotes activation of the behavioral immune system. Participants who had recently been ill, and had therefore recently experienced activation of their biological immune system, in one study displayed heightened attention to disfigured individuals, and in a second study showed avoidance — cognitive and behavioral processes reflecting activation of the behavioral immune system. These findings shed light on the interactive nature of biological and psychological mechanisms designed to help people overcome the threat of disease.

Heirarchies of empathy in the brain

Following the previous post I thought it would be useful to pass on more of Panskepp's review, which provides a more general description:

There is a growing recognition of how animals respond to the affective states of other animals, including the show of empathy, a state once thought to be unique to primates...A key question concerns the nature of the rats' motivations—the affective and cognitive underpinnings of their “empathy.” ...Future research needs to untangle whether empathic responses in mammals arise more from higher cognitive or lower affective brain functions, or some combination of these (see the figure). Human brain imaging studies of empathy suggest both are involved, especially in coping with the distress of others. But solid neurobiologically based evolutionary evidence, both bottom-up and top-down, is so far lacking.

Figure legend - One concept of how mammalian brains generate empathic responses at different levels is shown. Primary emotional processes, where sources of empathy may arise (i.e., feeling what other organisms are feeling), coordinate with secondary-process learning and memory mechanisms (i.e., knowing what others are feeling). Both of these then interact with higher mental processes, which can exert a variety of top-down influences on the regulation of empathic tendencies (i.e., desires to respond compassionately to others' distress).

The layering of evolutionary progressions is evident in the human brain. The deepest midbrain and hypothalamic regions mediate primary-process, instinctual affects. More recently evolved subcortical regions, among them basal ganglia, amygdala, and nucleus accumbens, help promote higher cognitive activities through learning and memory. Although we currently look to mirror-neuron zones of the neocortex for evidence of the highest mind functions such as compassion, empathic tendencies are surely also promoted by the more ancient primary-process emotional networks that are essential foundations for mental life. For example, a primal form of “empathy” is mothers' exquisite sensitivity to crying babies. Might crying access those systems in mothers' brains that are known to mediate separation anxiety in young animals? Perhaps affective urges for maternal caregiving are triggered as mothers' brains experience psychological pain engendered by their infants' cries. It may be that empathic coordination of social motivations is mediated by emotional resonances among nearby animals, allowing receivers to experience the emotions of transmitters. At such deep affective levels, emotional states may reverberate among animals, with no need for learned rerepresentations arising from mirror neurons. Mammals may have intrinsic abilities to resonate with the pains and joys of nearby others through primal emotional contagion. 

Much deep-brain research remains to be done to understand the degree to which mammalian empathy is achieved more through higher social-cognitive processes or primal affective processes in the brain. Simplified models of empathy, as in mice and rats, offer new inroads for understanding our own social-emotional nature and nurture. Such knowledge may eventually help us promote nurturant behaviors in humans.

Empathy in rats - a great video

Bartal et al. show yet another example of how the kind of empathic concern humans can show for others is already developed in the rat, a much more simple mammal. I pass on the summary of the work in Science, and be sure to watch the really excellent instructional video the authors provide, showing how a free rat overcomes the fear (caused by emotional contagion from a distressed rat trapped in a small plastic box) to open a door to let the trapped rats escape:

Empathy, a well-known characteristic in humans, occurs when an individual is motivated to help another, while maintaining emotional separation. Thus, it is distinct from emotional contagion where an individual begins to experience the emotions of other individuals, and act similarly. Emotional contagion is known to occur in many mammalian species, but empathy has often been considered unique to primates. Through a controlled experiment in captive rats, Ben-Ami Bartal et al. (p. 1427; see the Perspective by Panksepp) show that the biological roots of empathy could be much deeper than recognized. Rats were highly motivated to release a restrained cagemate, even when they were not permitted any immediate contact with it after release. Furthermore, when presented with chocolate, a highly preferred food, the rats were still motivated to release their cagemate and even shared the food with them. Thus, empathically motivated prosocial behavior is not limited to primates, and—like many other behaviors previously thought to be limited to this group—may serve similarly important functions across species.

Chemical and social mechanisms of self healing.

Two fascinating recent articles deal with the power we seem to have to heal ourselves by believing that a particular faith, meditation, or procedure (like acupuncture or an effective looking sugar pill) will do the job. An article by Michael Specter in the Dec. 12 issue of the New Yorker describes the work of Ted Kaptchuk, who is director of the Harvard Program in Placebo Studies and the Therapeutic Encounter. The second article, by Nicholas Humphrey, suggests that the placebo effect is the result of a trick that has been played by human culture, and that is can be generalized to explain how we might also be able to alter our 'self-management systems'.

The Specter article gives a nuanced discussion of the complexity and ambiguities of alternative healing treatments. I am amazed that I had not been aware of results of neuroimaging studies that have tracked brain activity in response to either a drug or a placebo as soon as they are taken. One has shown that injection of saline that has been described as a drug can reduce a patient's symptoms of Parkinson's disease and caused in crease in brain dopamine that the disease destroys. A chemical basis of a pain relieving placebo effect was shown in a seminal 1978 experiment in which dental surgery patients who reported their pain was decreased by receiving an injection of saline instead of morphine had Naloxone added to their I.V. drips. Naloxone is a drug developed to counteract overdoses of heroin and morphine by blocking opioid receptors in the central nervous system that are normally acted on by endorphins. Naloxone blocked the placebo pain relief, proving that its chemical basis was most likely due to the actual relief of endorphins in the brain by the power of belief.

It appears that when we think we are receiving a drug that is capable of changing the level of a molecule that our body can manufacture (dopamine or endorphins in the examples just given) our body goes ahead and changes those levels by itself. There is objective chemical evidence that we can "heal ourselves". (The flip side of this is the "Nocebo Effect", in which the suggestion that a procedure is going to be painful actually cause it to be so, or enhance it.)

The Humphrey article looks at the larger context that he suggest enables these phenomena, and the reason that faith healing and medicine could be as effective as they were become they had any rational or scientific basis. Some edited chunks:

...until less than 100 years ago, there was hardly anything a doctor could do that would be effective in any physiological medicinal way—and still the doctor's ministrations often "worked". That's to say, under the influence of what we would today call placebo medicine people came to feel less pain, to experience less fever, their inflammations receded, and so on...I realized it must be the result of a trick that has been played by human culture. The trick isto persuade sick people that they have a "license" to get better, because they'rein the hands of supposed specialists who know what's best for them and can offer practical help and reinforcements. And the reason this works is that it reassures people—subconsciously —that the costs of self-cure will be affordable and that it's safe to let down their guard. So health has improved because of a cultural subterfuge. It's been a pretty remarkable development.

Noting the overwhelming evidence that our character is molded by sub-conscious environmental and cultural cues he continues:

To explain placebos I think we need to invoke the existence of an "evolved health management system". The placebo effect is a particular kind of priming effect. And what I want to do now is to explain a whole range of other priming effects by invoking the existence of an "evolved self-management system".

It makes sense that our brains should have come to play a crucial part in the top-down management of bodily health. As I see it, what the health management system has evolved to do is to perform a kind of economic analysis of what the opportunities and the costs of cure will be: what resources we've got in reserve, how dangerous the situation is right now, what predictions we can make of what the future holds...So now, where does the placebo effect fit in? Placebos work because they suggest to people that the picture is rosier than it really is. Just like the artificial summer light cycle for the hamster - which causes them to mount a more massive and effective immune response to infection, because it is not as important to conserve resources in the summer as in the winter - placebos give people fake information that it's safe to cure them. Whereupon they do just that.

This suggests we should see the placebo effect as part of a much larger picture of homeostasis and bodily self-control. But now I'm ready to expand on this much further still. If this is the way humans and animals manage their physical health, there must surely be a similar story to be told about mental health. And if mental health, then—at least with humans—it should apply to personality and character as well. So I've come round to the idea that humans have in fact evolved a full-blown self management system, with the job of managing all their psychological resources put together, so as to optimise the persona they present to the world...our ancestors already had a template for doing these calculations, namely the pre-existing health system. In fact I believe the self management system evolved on the back of the health system. But this new system goes much further than the older one: it's job is to read the local signs and signs and forecast the psychological weather we are heading into, enabling us to prejudge what we can get away with, what's politic, what's expected of us. Not surprisingly, it's turned out to be a very complex system. That's why psychologists working on priming are discovering so many cues, which are relevant to it. For there are of course so many things that are relevant to managing our personal lives and coming across in the most effective and self-promoting ways we can.

Because our circumstances have generally improved in the last ten thousand years, and yet evolutionary catch-up occurs relatively slowly, this means that both systems will have become "out of date" in the way they calculate costs and benefits. At both the health-level and the self-level, there are bound to be things humans could not risk doing in the past that they can risk now.

Placebo medication works by tricking the subject with false information into believing the situation warrants a reduction in pain, for example, or the mounting of an expensive immune response. Yet it's precisely because our environment today is less dangerous than it used to be, that responding to this trick no longer puts us at an unacceptable risk...because the same kind of improvement has occurred in our social lives, the same goes for the risks with managing the self. In the "environment of evolutionary adaptiveness"—the social and physical environment, 100,000-10,000 years ago, in which many of our biological adaptations were laid down—our ancestors lived in very small scale societies, where individuals were monitored all the time by the group, and it was essential to conform to others' expectations...We no longer live in such an oppressive environment. We no longer need to play by the old rules, and rein in our peculiar strengths and idiosyncrasies. We can afford to take risks now we couldn't before...I think it really ought to be possible to devise placebo treatments for the self, which do indeed induce them to come out from their protective shells —and so to emerge as happier, nicer, cleverer, more creative people than they would ever otherwise have dared to be.

Perfecting the not quite perfect

I pass on this interesting item by Peter Stern from the Editor's choice section of Science Magazine:

Even the best musicians make slight errors when playing a rhythm. We find this frailty to be appealing, as evidenced by the fact that computer-generated perfect rhythms are often perceived as sterile or artificial. Having known this phenomenon for a long time, software engineers have added slight rhythmic fluctuations to make computer-generated music sound more human. These fluctuations are usually produced by a random number generator. Hennig et al. have now analyzed the statistical properties of music produced by professional musicians. They found that there are long-range fluctuations when humans produce all sorts of rhythms. A small rhythmic fluctuation at some point in time not only influenced fluctuations shortly thereafter, but even after tens of seconds. When given the choice, listeners clearly preferred music produced according to these criteria over the random number-generated fluctuations. The authors conclude that these results may not only have practical implications such as improved techniques for audio editing and humanizing music, but they may also provide new insights into the neurophysiology of time perception and timing of actions.

Here is the Hennig et al. abstract:

Although human musical performances represent one of the most valuable achievements of mankind, the best musicians perform imperfectly. Musical rhythms are not entirely accurate and thus inevitably deviate from the ideal beat pattern. Nevertheless, computer generated perfect beat patterns are frequently devalued by listeners due to a perceived lack of human touch. Professional audio editing software therefore offers a humanizing feature which artificially generates rhythmic fluctuations. However, the built-in humanizing units are essentially random number generators producing only simple uncorrelated fluctuations. Here, for the first time, we establish long-range fluctuations as an inevitable natural companion of both simple and complex human rhythmic performances. Moreover, we demonstrate that listeners strongly prefer long-range correlated fluctuations in musical rhythms. Thus, the favorable fluctuation type for humanizing interbeat intervals coincides with the one generically inherent in human musical performances.

REM sleep chills out amygdala, reduces emotional reactivity

van der Helm et al. at Univ. of Cal. Berkeley have done interesting experiments in which 34 adults were randomly assigned to two groups which both performed an emotion reactivity test twice inside a functional magnetic resonance imaging (fMRI) scanner; separated by a 12 hr interval. The tests involved the rating and subsequent rerating of the same standard set of 150 affective picture stimuli. One group slept during the twelve hours interval with REM (rapid eye movement) sleep monitored by EEG, the other group was a control group that stayed awake during the day. Controls were done to eliminate possible time-of-day differences in emotional reactivity, independent of wake or sleep. Here is their abstract:

Clinical evidence suggests a potentially causal interaction between sleep and affective brain function; nearly all mood disorders display co-occurring sleep abnormalities, commonly involving rapid-eye movement (REM) sleep. Building on this clinical evidence, recent neurobiological frameworks have hypothesized a benefit of REM sleep in palliatively decreasing next-day brain reactivity to recent waking emotional experiences. Specifically, the marked suppression of central adrenergic neurotransmitters during REM (commonly implicated in arousal and stress), coupled with activation in amygdala-hippocampal networks that encode salient events, is proposed to (re)process and depotentiate previous affective experiences, decreasing their emotional intensity. In contrast, the failure of such adrenergic reduction during REM sleep has been described in anxiety disorders, indexed by persistent high-frequency electroencephalographic (EEG) activity (greater than 30 Hz); a candidate factor contributing to hyperarousal and exaggerated amygdala reactivity. Despite these neurobiological frameworks, and their predictions, the proposed benefit of REM sleep physiology in depotentiating neural and behavioral responsivity to prior emotional events remains unknown. Here, we demonstrate that REM sleep physiology is associated with an overnight dissipation of amygdala activity in response to previous emotional experiences, altering functional connectivity and reducing next-day subjective emotionality.

How exercise benefits the brain - importance of BNDF

Gretchen Reynolds summarizes several experiments demonstrating that exercise stimulates synthesis of brain derived neurotropic factor (BNDF), which promotes the health and multiplication of brain cells, and apparently also cognitive health. An Irish group has shown that strenuous aerobic exercise on a stationary cycle boosts BNDF levels and also performance on memory tests. A Brazilian group found that after sedentary elderly rats ran for approximately five minutes several days a week for five weeks, BNDF production increased in memory center of their brains. The old, exercised animals then performed almost as well as much younger rats on rodent memory tests. A study at UCLA showed that if adult rats were allowed to run at will for a week, the memory centers of their brains afterward contained more BDNF molecules than those of sedentary rats. Finally a Stanford study found that the normally occurring decay of performance with age in skilled airline pilots was more pronounced in those who carried a common genetic variation that is believed to reduce BDNF activity in their brains.

Psychopathy correlates with reduced prefrontal connectivity.

Psychopathy, defined as callous and impulsive antisocial behavior, is present in approximately a quarter of adult prison inmates. For many years, it has been known that changes accompanying ventro-medial prefrontal cortex (vmPFC) damage (lack of empathy, irresponsibility, and poor decision making) bear striking resemblance to psychopathic personality traits. Motzkin et al have now used two complementary neuroimaging methods to quantify the structural and functional connectivity of vmPFC in 27 psychopathic and non-psychopathic prison inmates. Their abstract:

Linking psychopathy to a specific brain abnormality could have significant clinical, legal, and scientific implications. Theories on the neurobiological basis of the disorder typically propose dysfunction in a circuit involving ventromedial prefrontal cortex (vmPFC). However, to date there is limited brain imaging data to directly test whether psychopathy may indeed be associated with any structural or functional abnormality within this brain area. In this study, we employ two complementary imaging techniques to assess the structural and functional connectivity of vmPFC in psychopathic and non-psychopathic criminals. Using diffusion tensor imaging, we show that psychopathy is associated with reduced structural integrity in the right uncinate fasciculus, the primary white matter connection between vmPFC and anterior temporal lobe. Using functional magnetic resonance imaging, we show that psychopathy is associated with reduced functional connectivity between vmPFC and amygdala as well as between vmPFC and medial parietal cortex. Together, these data converge to implicate diminished vmPFC connectivity as a characteristic neurobiological feature of psychopathy.

Purging senescent cells can prevent some ills of aging.

I've held off on noting some recent work relevant to longevity that has received quite a lot of press, because I increasingly rebel at the enormous amount of effort going into life extension. It is hard, however, to not be interested in experiments that appear relevant to enhancing the quality of a normal life span, so that health and robustness are maintained until a system failure rapidly takes down the whole show. The report by Baker et al. examines cells that have stopped dividing (senescent cells) and hasten aging in the tissues in which they accumulate (like my arthritic knees!) by secreting agents that stimulate low-level inflammation. Barker et al. use a neat genetic trick (not yet available to us humans) to eliminate senescent cells in mice. From Wade's summary:

...senescent cells...reliably switch on a characteristic marker gene known as p16-Ink4a. [Barker et al.]... arranged that the genetic element that switches on the marker gene would also prime a mechanism to make the cell self-destruct. The mechanism fired only when the mice were dosed with a specific drug. The result was that only senescent cells were at risk from the drug...they could be purged at any desired time in the mouse’s lifetime.

Life-long removal of senescent cells delayed the onset of age-related pathologies in fat,skeletal muscle, and eye tissues, and clearance in late life attenuated the progression of these pathologies (such as cataracts). So, it appears that removal of senescent cells can prevent or delay tissue dysfunction and should extend lifespan.

Ignoring the bad news...the brain’s rose colored glasses

Dolan and Colleagues have done yet another fascinating piece of work, showing brain activity that correlates with the tendency of people to remain overly optimistic even when faced with information about a gloomy future (optimism bias). This is another example of 'not attending to bad news' (noted in a mindblog post last week as underlying some people having less ability to learn from their mistakes). The Sharot et al. study shows that people are selectively worse at incorporating information about a worse-than-expected future, and describes the learning signals in the brain that correlate with this bias:

Unrealistic optimism is a pervasive human trait that influences domains ranging from personal relationships to politics and finance. How people maintain unrealistic optimism, despite frequently encountering information that challenges those biased beliefs, is unknown. We examined this question and found a marked asymmetry in belief updating. Participants updated their beliefs more in response to information that was better than expected than to information that was worse. This selectivity was mediated by a relative failure to code for errors that should reduce optimism. Distinct regions of the prefrontal cortex tracked estimation errors when those called for positive update, both in individuals who scored high and low on trait optimism. However, highly optimistic individuals exhibited reduced tracking of estimation errors that called for negative update in right inferior prefrontal gyrus. These findings indicate that optimism is tied to a selective update failure and diminished neural coding of undesirable information regarding the future.

A gene that makes you appear to be kinder...

Kogan and colleagues at the Univ. of Toronto have examined some behavioral consequences of variations of the gene that codes for the receptor for the hormone oxytocin, since high levels of oxytocin are believed to make people more sociable. Volunteers (116) were asked to watch 23 brief silent videos that showed people with GG, GA, or AA versions of the gene responding to their partner telling them a story of personal suffering, and rate how kind and trustworthy the person in the video appeared to be. Those with the homozygous GG version of the oxytocin receptor gene were judged to be kinder than those with GA or AA versions, apparently because those with GG variations used significantly more non-verbal empathetic gestures in their storytelling such as smiling and nodding. Here is the abstract:

Individuals who are homozygous for the G allele of the rs53576 SNP of the oxytocin receptor (OXTR) gene tend to be more prosocial than carriers of the A allele. However, little is known about how these differences manifest behaviorally and whether they are readily detectable by outside observers, both critical questions in theoretical accounts of prosociality. In the present study, we used thin-slicing methodology to test the hypotheses that (i) individual differences in rs53576 genotype predict how prosocial observers judge target individuals to be on the basis of brief observations of behavior, and (ii) that variation in targets’ nonverbal displays of affiliative cues would account for these judgment differences. In line with predictions, we found that individuals homozygous for the G allele were judged to be more prosocial than carriers of the A allele. These differences were completely accounted for by variations in the expression of affiliative cues. Thus, individual differences in rs53576 are associated with behavioral manifestations of prosociality, which ultimately guide the judgments others make about the individual.

Why does synesthesia persist in the population?

Brang and Ramachandran do an interesting review of ideas on synesthesia, a condition present in 2%–4% of the population,in which a sensory stimulus presented to one modality elicits concurrent sensations in additional modalities. In two of the most common variants, auditory tones and achromatic (colorless) numbers produce vivid and perceptually salient colors. The authors point out that synesthesia can be associated with a wide variety of conceptual and perceptual benefits, suggesting that the gene(s) involved may have been selected for because of a hidden agenda. They speculate that increasing the range of sensory associations may extend to other systems such as creativity and metaphor (increasing the range of association between words). They point to examples of people with prodigious memories based largely on using synesthetic associations evoked by the items to be memorized.

In addition to facilitating processes in individual sensory modalities, synesthetes also show increased communication between the senses unrelated to their synesthetic experiences, suggesting that benefits from synesthesia generalize to other modalities as well, supporting their ability to process multisensory information. Furthermore, others have argued that synesthesia is the direct result of enhanced communication between the senses as a logical outgrowth of the cross-modality interactions present in all individuals. Taken collectively, these data suggest that synesthesia may be associated with enhanced primary sensory processing as well as the integration between the senses...synesthesia is a highly heritable phenomenon that is associated with numerous benefits to cognitive processing, potentially underscoring a basis for why this condition has survived evolutionary pressures.

Our brain's fusiform "face" area is about holistic processing of any familiar complex visual input.

As a followup to an older MindBlog post on Chess expertise, I though I would pass on this interesting work from Bilalić et al.

The fusiform face area (FFA) is involved in face perception to such an extent that some claim it is a brain module for faces exclusively. The other possibility is that FFA is modulated by experience in individuation in any visual domain, not only faces. Here we test this latter FFA expertise hypothesis using the game of chess as a domain of investigation. We exploited the characteristic of chess, which features multiple objects forming meaningful spatial relations. In three experiments, we show that FFA activity is related to stimulus properties and not to chess skill directly. In all chess and non-chess tasks, experts' FFA was more activated than that of novices' only when they dealt with naturalistic full-board chess positions. When common spatial relationships formed by chess objects in chess positions were randomly disturbed, FFA was again differentially active only in experts, regardless of the actual task. Our experiments show that FFA contributes to the holistic processing of domain-specific multipart stimuli in chess experts. This suggests that FFA may not only mediate human expertise in face recognition but, supporting the expertise hypothesis, may mediate the automatic holistic processing of any highly familiar multipart visual input.

Neural (MRI) correlates of effective learning.

Here is a rather fascinating prospective use of MRI technology - to distinguish people who might become the most effective decision makers after further more extensive training in a specialization such as medical diagnosis. Their basic finding is that high performers' brains achieve better outcomes by attending to informative failures during training, rather than chasing the reward value of successes. From Downar, Bhatt, and Montague:

Accurate associative learning is often hindered by confirmation bias and success-chasing, which together can conspire to produce or solidify false beliefs in the decision-maker. We performed functional magnetic resonance imaging in 35 experienced physicians, while they learned to choose between two treatments in a series of virtual patient encounters. We estimated a learning model for each subject based on their observed behavior and this model divided clearly into high performers and low performers. The high performers showed small, but equal learning rates for both successes (positive outcomes) and failures (no response to the drug). In contrast, low performers showed very large and asymmetric learning rates, learning significantly more from successes than failures; a tendency that led to sub-optimal treatment choices. Consistently with these behavioral findings, high performers showed larger, more sustained BOLD responses to failed vs. successful outcomes in the dorsolateral prefrontal cortex and inferior parietal lobule while low performers displayed the opposite response profile. Furthermore, participants' learning asymmetry correlated with anticipatory activation in the nucleus accumbens at trial onset, well before outcome presentation. Subjects with anticipatory activation in the nucleus accumbens showed more success-chasing during learning. These results suggest that high performers' brains achieve better outcomes by attending to informative failures during training, rather than chasing the reward value of successes. The differential brain activations between high and low performers could potentially be developed into biomarkers to identify efficient learners on novel decision tasks, in medical or other contexts.

The speed-accuracy tradeoff in the elderly brain.

Sigh...even more information on my aging brain. The fact that I and other older folks take longer to respond when a task is presented can most charitably be attributed to our being more cautious about making errors, but Forstmann et al. find evidence that this behavior is not entirely voluntary, and can also be related to a decrease in brain connectivity with aging:

Even in the simplest laboratory tasks older adults generally take more time to respond than young adults. One of the reasons for this age-related slowing is that older adults are reluctant to commit errors, a cautious attitude that prompts them to accumulate more information before making a decision. This suggests that age-related slowing may be partly due to unwillingness on behalf of elderly participants to adopt a fast-but-careless setting when asked. We investigate the neuroanatomical and neurocognitive basis of age-related slowing in a perceptual decision-making task where cues instructed young and old participants to respond either quickly or accurately. Mathematical modeling of the behavioral data confirmed that cueing for speed encouraged participants to set low response thresholds, but this was more evident in younger than older participants. Diffusion weighted structural images suggest that the more cautious threshold settings of older participants may be due to a reduction of white matter integrity in corticostriatal tracts that connect the pre-SMA to the striatum. These results are consistent with the striatal account of the speed-accuracy tradeoff according to which an increased emphasis on response speed increases the cortical input to the striatum, resulting in global disinhibition of the cortex. Our findings suggest that the unwillingness of older adults to adopt fast speed-accuracy tradeoff settings may not just reflect a strategic choice that is entirely under voluntary control, but that it may also reflect structural limitations: age-related decrements in brain connectivity.

How not to revert to habit under stress...

A stressful situation can have the effect of making us actually less able to flexibly cope with the issue at hand, because we tend under stress to regress to older habitual responses that may be less appropriate. Observations by Schwabe et al. suggest that we might be able to lessen this behavior by popping an old fashioned pill like propanolol, a β-adrenoceptor antagonist (which has been used for many years by some musicians to quell their performance anxiety). The second abstract below, from Hermans et al. provides a more detailed view of how our brain networks are changing during stress, and how this is attenuated by β-adrenoceptor receptor blockage.

Stress modulates instrumental action in favor of habit processes that encode the association between a response and preceding stimuli and at the expense of goal-directed processes that learn the association between an action and the motivational value of the outcome. Here, we asked whether this stress-induced shift from goal-directed to habit action is dependent on noradrenergic activation and may therefore be blocked by a β-adrenoceptor antagonist. To this end, healthy men and women were administered a placebo or the β-adrenoceptor antagonist propranolol before they underwent a stress or a control procedure. Shortly after the stress or control procedure, participants were trained in two instrumental actions that led to two distinct food outcomes. After training, one of the food outcomes was selectively devalued by feeding participants to satiety with that food. A subsequent extinction test indicated whether instrumental behavior was goal-directed or habitual. As expected, stress after placebo rendered participants' behavior insensitive to the change in the value of the outcome and thus habitual. After propranolol intake, however, stressed participants behaved, same as controls, goal-directed, suggesting that propranolol blocked the stress-induced bias toward habit behavior. Our findings show that the shift from goal-directed to habitual control of instrumental action under stress necessitates noradrenergic activation and could have important clinical implications, particularly for addictive disorders.

And, more detail from Hermans et al., who find in human studies robust stressor-related changes in functional neuronal activity and connectivity within a network of brain areas, which correlate with increased reports of negative emotionality by the participants, as well as with increases of cortisol and alpha amylase in their saliva:

Acute stress shifts the brain into a state that fosters rapid defense mechanisms. Stress-related neuromodulators are thought to trigger this change by altering properties of large-scale neural populations throughout the brain. We investigated this brain-state shift in humans. During exposure to a fear-related acute stressor, responsiveness and interconnectivity within a network including cortical (frontoinsular, dorsal anterior cingulate, inferotemporal, and temporoparietal) and subcortical (amygdala, thalamus, hypothalamus, and midbrain) regions increased as a function of stress response magnitudes. β-adrenergic receptor blockade, but not cortisol synthesis inhibition, diminished this increase. Thus, our findings reveal that noradrenergic activation during acute stress results in prolonged coupling within a distributed network that integrates information exchange between regions involved in autonomic-neuroendocrine control and vigilant attentional reorienting.

A nap enhances relational memory

Lau et al. make the following interesting observations:

It is increasingly evident that sleep strengthens memory. However, it is not clear whether sleep promotes relational memory, resultant of the integration of disparate memory traces into memory networks linked by commonalities. The present study investigates the effect of a daytime nap, immediately after learning or after a delay, on a relational memory task that requires abstraction of general concept from separately learned items. Specifically, participants learned English meanings of Chinese characters with overlapping semantic components called radicals. They were later tested on new characters sharing the same radicals and on explicitly stating the general concepts represented by the radicals. Regardless of whether the nap occurred immediately after learning or after a delay, the nap participants performed better on both tasks. The results suggest that sleep – even as brief as a nap – facilitates the reorganization of discrete memory traces into flexible relational memory networks.

Brief musical training in kids enhances other high level cognitive skills.

Article like this one from Moreno et al. make me think that my life long piano practice may be part of the reason I'm still hanging onto a few of my mental marbles as I age. (I realized the other day that my sight reading of complex musical scores, which requires glancing several measures ahead of the one being played, and remembering them, is essentially working memory training of the sort that has been shown to enhance general intelligence.) Here is the abstract from Moreno et al:

Researchers have designed training methods that can be used to improve mental health and to test the efficacy of education programs. However, few studies have demonstrated broad transfer from such training to performance on untrained cognitive activities. Here we report the effects of two interactive computerized training programs developed for preschool children: one for music and one for visual art. After only 20 days of training, only children in the music group exhibited enhanced performance on a measure of verbal intelligence, with 90% of the sample showing this improvement. These improvements in verbal intelligence were positively correlated with changes in functional brain plasticity during an executive-function task. Our findings demonstrate that transfer of a high-level cognitive skill is possible in early childhood.