Cultural specificity in amygdala response to fear faces

From Chiao et al. :

The human amygdala robustly activates to fear faces. Heightened response to fear faces is thought to reflect the amygdala's adaptive function as an early warning mechanism. Although culture shapes several facets of emotional and social experience, including how fear is perceived and expressed to others, very little is known about how culture influences neural responses to fear stimuli. Here we show that the bilateral amygdala response to fear faces is modulated by culture. We used functional magnetic resonance imaging to measure amygdala response to fear and nonfear faces in two distinct cultures. Native Japanese in Japan and Caucasians in the United States showed greater amygdala activation to fear expressed by members of their own cultural group. This finding provides novel and surprising evidence of cultural tuning in an automatic neural response.

The innovative brain

Lawrence et al. present preliminary neurocognitive data from matched groups of entrepreneurs and managerial controls that suggests that entrepreneurs represent an example of highly adaptive risk-taking behavior, with positive functional outcomes in the context of stressful economic decision-making. They suggest this 'functional impulsivity' may have evolutionary value as a means of seizing opportunities in a rapidly changing environment. Their neurocognitive tests distinguished the involvement of distinct processes in risky and risk-free decision-making. Referred to as 'hot' and 'cold' processes, these appear to be localized to distinct regions of the brain's frontal lobes. Risk-taking performance in the entrepreneurs was accompanied by elevated scores on personality impulsiveness measures and superior cognitive-flexibility performance. They conclude that entrepreneurs and managers do equally well when asked to perform cold decision-making tasks, but differences emerge in the context of risky or emotional decisions.

The pattern of performance seen on a gambling task in entrepreneurs reflects a behavioral index of risk-seeking or risk tolerance. Greater rewards (as well as greater losses) are available for those who bet more. If these impulsive risk-taking traits can be beneficial, can they be taught or otherwise imparted to the potential entrepreneur? What does it take to make an entrepreneur — is it an inherited, inbuilt characteristic, or is it acquired, and if so, can it be acquired by anyone? These cognitive processes are intimately linked to brain neurochemistry, particularly to the neurotransmitter dopamine. Using single-dose psychostimulants to manipulate dopamine levels, we have seen modulation of risky decision-making on this task9. Therefore, it might be possible to enhance entrepreneurship pharmacologically.

Alexithymia

I just learned a new word: Alexithymia, the inability to express feelings with words, or more generally deficiency in understanding, processing, or describing emotions. The condition is associated with less activation of the anterior cingulate cortex, involved in cognitive and emotional processing. Gu et al. show that the trait is also associated with less efficient voluntary control.

Mozart's Symphony No. 40 in G minor - a new version

I just have to pass this on (from Andrews Sullivan's blog):

Towards a Moral Neuropolitics

Gary Olson writes an article on the neuroscience of empathy and mirror neuron systems, arguing that the morality that leads to progressive political possibilities is grounded in biology.

Making your tennis racquet part of your brain's body representation

Interesting work from Fourkas et al. in Cerebral Cortex:

Specific physical or mental practice may induce short- and long-term neuroplastic changes in the motor system and cause tools to become part of one's own body representation. Athletes who use tools as part of their practice may be an excellent model for assessing the neural correlates of possible bodily representation changes that are specific to extensive practice. We used single-pulse transcranial magnetic stimulation to measure corticospinal excitability in forearm and hand muscles of expert tennis players and novices while they mentally practiced a tennis forehand, table tennis forehand, and a golf drive. The muscles of expert tennis players showed increased corticospinal facilitation during motor imagery of tennis but not golf or table tennis. Novices, although athletes, were not modulated across sports. Subjective reports indicated that only in the tennis imagery condition did experts differ from novices in the ability to form proprioceptive images and to consider the tool as an extension of the hand. Neurophysiological and subjective data converge to suggest a key role of long-term experience in modulating sensorimotor body representations during mental simulation of sports.

Why do intelligent people live longer?

Ian Deary offers an interesting essay in Nature. Here are some clips:

Scores from cognitive-ability tests (intelligence tests or IQ tests) have validity that is almost unequalled in psychology. A general cognitive-ability factor emerges from measures of diverse mental tasks, something that hundreds of data sets since 1904 have replicated. People's rankings on intelligence tests show high stability across almost the whole lifespan, are substantially heritable and are associated with important life outcomes — including educational achievements, occupational success and morbidity and mortality. More thumping confirmatory studies of the link between intelligence and mortality have appeared...One of these contains nearly a million Swedish men tested at around age 19 during military induction and followed for almost 20 years. It shows a clear association: as intelligence test scores go up the scale, so too does the likelihood of survival over those two decades...Intelligence can predict mortality more strongly than body mass index, total cholesterol, blood pressure or blood glucose, and at a similar level to smoking4. But the reasons for this are still mysterious.

The field has focused on four non-exclusive possibilities for the link between intelligence and death. First, what occurs to many people as an obvious pathway of explanation, is that intelligence is associated with more education, and thereafter with more professional occupations that might place the person in healthier environments. Statistical adjustment for education and adult social class can make the association between early-life intelligence and mortality lessen or disappear. But not always.

Second, people with higher intelligence might engage in more healthy behaviours. Evidence is accruing that people with higher intelligence in early life are more likely to have better diets, take more exercise, avoid accidents, give up smoking, engage in less binge drinking and put on less weight in adulthood. But this too doesn't seem to be the whole story.

Third, mental test scores from early life might act as a record of insults to the brain that have occurred before that date. These insults — perinatal events, or the result of illnesses, accidents or deprivations before the mental testing — might be the fundamental cause behind both intelligence test scores and mortality risk. So far, little evidence supports this.

Fourth, mental test scores obtained in youth might be an indicator of a well-put-together system. It is hypothesized that a well-wired body is more able to respond effectively to environmental insults. This 'system integrity' idea has a parallel in the field of ageing, where some data suggest that bodily and cognitive functions age in concert. Some supporting evidence comes from the finding that simple reaction speed — the time taken to press a button when a stimulus appears — can displace intelligence test scores as an even better predictor of mortality risk.

There is also a search for other, non-cognitive psychological characteristics that are associated with living longer. For example, it seems that, independently of any association with intelligence, being more dependable or conscientious in childhood is also significantly protective to health. Children who scored in the top 50% of the population for intelligence and dependability were in one study more than twice as likely to survive to their late sixties as children scoring in the bottom half for both.

Religion and visual attention

Colzato et al. report a quirky study in PLoS ONE: "Losing the Big Picture: How Religion May Control Visual Attention"

Despite the abundance of evidence that human perception is penetrated by beliefs and expectations, scientific research so far has entirely neglected the possible impact of religious background on attention. Here we show that Dutch Calvinists and atheists, brought up in the same country and culture and controlled for race, intelligence, sex, and age, differ with respect to the way they attend to and process the global and local features of complex visual stimuli: Calvinists attend less to global aspects of perceived events, which fits with the idea that people's attentional processing style reflects possible biases rewarded by their religious belief system.

The way we age

I find myself returning again and again to a New Yorker article by Atul Gawande, "The Way We Age Now." (PDF here). It was the subject of a May 2007 post which included a few clips from the article. His descriptions of the natural processes that underlie changes in teeth, hair, skin, bones, muscles, joints, etc during agin are the most concise and clear that I have read.

Massive reorganization of visual cortex at the level of dendritic spines..

Keck et al. do elegant experiments to directly observe spine replacement in individual apical dendritic tufts of layer-5 pyramidal neurons, replacement that correlates with functional recovery over a period of months after lesioning the retinal input:

The cerebral cortex has the ability to adapt to altered sensory inputs. In the visual cortex, a small lesion to the retina causes the deprived cortical region to become responsive to adjacent parts of the visual field. This extensive topographic remapping is assumed to be mediated by the rewiring of intracortical connections, but the dynamics of this reorganization process remain unknown. We used repeated intrinsic signal and two-photon imaging to monitor functional and structural alterations in adult mouse visual cortex over a period of months following a retinal lesion. The rate at which dendritic spines were lost and gained increased threefold after a small retinal lesion, leading to an almost complete replacement of spines in the deafferented cortex within 2 months. Because this massive remodeling of synaptic structures did not occur when all visual input was removed, it likely reflects the activity-dependent establishment of new cortical circuits that serve the recovery of visual responses.

A novel theory of mental disorders

Benedict Carey writes a useful article on a radical new theory for explaining the psychotic spectrum:

...that an evolutionary tug of war between genes from the father’s sperm and the mother’s egg can, in effect, tip brain development in one of two ways. A strong bias toward the father pushes a developing brain along the autistic spectrum, toward a fascination with objects, patterns, mechanical systems, at the expense of social development. A bias toward the mother moves the growing brain along what the researchers call the psychotic spectrum, toward hypersensitivity to mood, their own and others’. This, according to the theory, increases a child’s risk of developing schizophrenia later on, as well as mood problems like bipolar disorder and depression.

In short: autism and schizophrenia represent opposite ends of a spectrum that includes most, if not all, psychiatric and developmental brain disorders. The theory has no use for psychiatry’s many separate categories for disorders, and it would give genetic findings an entirely new dimension.

The theory leans heavily on the work of David Haig of Harvard. It was Dr. Haig who argued in the 1990s that pregnancy was in part a biological struggle for resources between the mother and unborn child. On one side, natural selection should favor mothers who limit the nutritional costs of pregnancy and have more offspring; on the other, it should also favor fathers whose offspring maximize the nutrients they receive during gestation, setting up a direct conflict.

I strongly recommend that you read the article, which goes on to give a lucid explanation of how gene imprinting regulates this competition.

Language evolution embedded in cooperative social context

Another installment in the Nature series "Being Human" is offered by Szathmáry and Számadó , who put the case that language evolved in a highly social, cooperative context as one of a suite of uniquely human traits, meriting special status because of the opportunities that it opened up.

The subliminal power of logos

An interesting article by Rob Walker in the New York Times Magazine: "The Brand-ness of Strangers."

In one study, each subject was shown 20 photographs of people in various situations and instructed to focus on facial expressions. Afterward, each subject was offered a bottle of water from a selection of four brands. The experiment had nothing to do with facial expressions and everything to do with which kind of water they chose: the subjects had been divided into groups, based on how many of the photos they viewed incidentally included a bottle of Dasani water. Among those who looked at Dasani-free pictures, about 17 percent chose that brand. But about 40 percent of those who viewed a group of pictures that included 12 with a Dasani presence made the brand their pick. Since subjects who actually noticed the brand in the pictures were eliminated from the results, that spike in popularity evidently came from exposure that the subjects weren’t even aware of.

He discusses the very successful Ralph Lauren logo

Needless to say, a successful logo like Polo’s isn’t easy to create. But having attained and maintained such a level of familiarity, that logo may now be as effective as any of Ralph Lauren’s seductive ads — and for exactly the opposite reason: Not because it catches our attention, but because it doesn’t.

Is the financial meltdown a guy thing?

Dobrzynski asks whether traders have become prisoners of their endocrine systems — ruled by testosterone, the elixir of male aggressiveness, during a bull market; and by cortisol, a steroid that helps the body deal with stress, when the bears take over.

From Genes to Social Behavior

The Nov. 7 issue of Science Magazine is a gold mine of articles on genetics and behavior. I'm giving you here a clip from from the introduction to this special issue by Jasny et al. that contains links to the individual articles.

When it comes to behavior, we have moved beyond genetic determinism. Our genes do not lock us into certain ways of acting; rather, genetic influences are complicated and mutable and are only one of many factors affecting behavior. In their editorial, Landis and Insel (p. 821) elaborate on this idea, explaining that proteins encoded by genes direct the formation of multicomponent neural circuits, which are the true substrates of behavior, as these circuits respond to internal and outside stimuli.

Why do we study the genetic underpinnings of behavior? One reason is to understand how certain behaviors evolve. Conserved neural pathways can be tied to the evolution of social behaviors (Robinson et al., p. 896), and the conserved peptides oxytocin and vasopressin regulate social cognition and reproductive behaviors in many species (Donaldson and Young, p. 900). In a News story, Pennisi focuses on a region of chromosome 17 that has a complicated pattern of evolution in humans and other primates and is linked in unexpected ways to various disorders, including mental retardation, learning disabilities, and dementias.

Genetics can help us understand why identical circumstances can elicit different behavioral responses among individuals. Genetic differences are reflected in variations in behavior; activation of distinct versions of a hormone receptor gene, an example Donaldson and Young present, results in monogamous behavior in one species of vole but not in another. Conversely, as Robinson et al. describe, insights from recent work show that perceiving social information--such as bird songs or dominance behavior from cichlid fish--from another individual of the same species can itself alter gene expression in the brain, with downstream effects on physiology and behavior.

The potent genetic tools available for Drosophila have uncovered many genes that, when deleted, disrupt behaviors. This, in turn, has allowed dissection of the neural circuits that control essential behaviors. One of the best understood is a social activity necessary for reproduction--stereotypical mating behavior--as outlined by Dickson (p. 904). Genetic methods have also led to the understanding of another class of behaviors: those driven by the circadian clock. The genetic basis of the clock was elegantly worked out in Drosophila, followed by a similar achievement in mice. The reasons for these successes are outlined by Takahashi in his Perspective (p. 909), in which he also explains what tools will be needed to attain similar advances for other behaviors in mice.

Humans are not as genetically tractable as mice or flies, and human behavior is not as stereotypical. Holden's News story on the strengths and shortcomings of genetic studies of personality illustrates this point (p. 892). So do Cotton and some members of the Human Variome Project community in a Policy Forum (p. 861) that describes how the genes and loci associated with disorders of the nervous system are a particular challenge to geneticists and clinical neurologists in need of reliable diagnostic tests. And in a Perspective on a critical human social activity--politics--Fowler and Schreiber (p. 912) argue that genetics and neurobiology have much to teach us about how our leaders are chosen.

Some believe that psychology is the last frontier of genetic analysis. This special section provides a sampling of our early explorations.

Suffering Souls

A fascinating article in The New Yorker by John Seabrook on the search for the roots of psychopathy, the condition of moral emptiness that affects between fifteen to twenty-five per cent of the North American prison population, and is believed by some psychologists to exist in one per cent of the general adult male population. (Female psychopaths are thought to be much rarer.) Psychopaths don’t exhibit the manias, hysterias, and neuroses that are present in other types of mental illness. Their main defect, what psychologists call “severe emotional detachment”—a total lack of empathy and remorse—is concealed, and harder to describe than the symptoms of schizophrenia or bipolar disorder. It focuses on the work of Kent Kiehl, who has installed an fMRI scanner in a New Mexico prison. His theory, published in Psychiatry Research, in 2006, is that psychopathy is caused by a defect in what he calls “the paralimbic system,” a network of brain regions, stretching from the orbital frontal cortex to the posterior cingulate cortex, that are involved in processing emotion, inhibition, and attentional control.

Most popular MindBlog posts...

I sometimes glance at several of the free services that offer to monitor activity on one's blog (Feedburner, Google Analytics, Quantcast, etc). I thought this compilation of the most widely read posts on this blog was interesting. You can find any of them by entering a few words of the title in the search box in the left column.


And, in this vein, here is the history of subscribers to the RSS feed of this blog:

Sleep loss produces false memories.

From Diekelmann et al. :

People sometimes claim with high confidence to remember events that in fact never happened, typically due to strong semantic associations with actually encoded events. Sleep is known to provide optimal neurobiological conditions for consolidation of memories for long-term storage, whereas sleep deprivation acutely impairs retrieval of stored memories. Here, focusing on the role of sleep-related memory processes, we tested whether false memories can be created (a) as enduring memory representations due to a consolidation-associated reorganization of new memory representations during post-learning sleep and/or (b) as an acute retrieval-related phenomenon induced by sleep deprivation at memory testing. According to the Deese, Roediger, McDermott (DRM) false memory paradigm, subjects learned lists of semantically associated words (e.g., “night”, “dark”, “coal”,…), lacking the strongest common associate or theme word (here: “black”). Subjects either slept or stayed awake immediately after learning, and they were either sleep deprived or not at recognition testing 9, 33, or 44 hours after learning. Sleep deprivation at retrieval, but not sleep following learning, critically enhanced false memories of theme words. This effect was abolished by caffeine administration prior to retrieval, indicating that adenosinergic mechanisms can contribute to the generation of false memories associated with sleep loss.

Undoing cocaine's consequences.

In animal experiments stressful and aversive conditions can enhance drug-seeking and drug intake, while stress-reducing manipulations and nondrug rewards can reduce such behaviors. The acquisition of addiction-related behaviors such as sensitization and drug self-administration is attenuated in animals housed in enriched environments containing novel toys, food, and conspecifics with which to interact, compared with those housed in standard laboratory conditions. But, how is this relevant to treating drug-addicted humans, who present for treatment only after drug use is acquired? Recent work by Solinas et al. now suggests that environmental enrichment can still exert its beneficial effects on addiction-related behaviors even after they are established. Their abstract:

Environmental conditions can dramatically influence the behavioral and neurochemical effects of drugs of abuse. For example, stress increases the reinforcing effects of drugs and plays an important role in determining the vulnerability to develop drug addiction. On the other hand, positive conditions, such as environmental enrichment, can reduce the reinforcing effects of psychostimulants and may provide protection against the development of drug addiction. However, whether environmental enrichment can be used to “treat” drug addiction has not been investigated. In this study, we first exposed mice to drugs and induced addiction-related behaviors and only afterward exposed them to enriched environments. We found that 30 days of environmental enrichment completely eliminates behavioral sensitization and conditioned place preference to cocaine. In addition, housing mice in enriched environments after the development of conditioned place preference prevents cocaine-induced reinstatement of conditioned place preference and reduces activation of the brain circuitry involved in cocaine-induced reinstatement. Altogether, these results demonstrate that environmental enrichment can eliminate already established addiction-related behaviors in mice and suggest that environmental stimulation may be a fundamental factor in facilitating abstinence and preventing relapse to cocaine addiction.

During learning - competition between two memory systems.

An interesting bit of work from Lee et al.:

The multiple memory systems framework proposes that distinct circuits process and store different sorts of information; for example, spatial information is processed by a circuit that includes the hippocampus, whereas certain forms of instrumental conditioning depend on the striatum. Disruption of hippocampal function can enhance striatum-dependent learning in some paradigms, which has been interpreted as evidence that these systems can compete with one another in an intact animal. However, it remains unclear whether such competition can occur in the opposite direction, as suggested by the multiple memory systems framework, or is unidirectional. We addressed this question using lesions and genetic manipulations in mice. Impairment of dorsal striatal function with either excitotoxic lesions or transgenic inhibition of the transcription factor cAMP response element-binding protein, which disrupts striatal synaptic plasticity, impaired striatum-dependent cued learning but enhanced hippocampus-dependent spatial learning. Conversely, excitotoxic lesions of the dorsal hippocampus disrupted spatial learning and enhanced cued learning. This double dissociation demonstrates bidirectional competition that constitutes strong evidence for the parallel operation of distinct memory systems.