Would Tarzan believe in God?

Some clips from Konika Banerjee and Paul Bloom:

Would someone raised without exposure to religious views nonetheless come to believe in the existence of God, an afterlife, and the intentional creation of humans and other animals? Many scholars would answer yes, proposing that universal cognitive biases generate religious ideas anew within each individual mind. Drawing on evidence from developmental psychology, we argue here that the answer is no: children lack spontaneous theistic views and the emergence of religion is crucially dependent on culture.

...if universal, early-emerging cognitive biases generate religious ideas, we would expect to see these ideas emerge spontaneously. This would be akin to the process of creolization, such as when deaf children who are exposed to non-linguistic communication systems create their own sign language. However, such cases are, as best we know, non-existent. There are many examples where children are quick to endorse religious beliefs, often surprising their atheist parents. But this is consistent with receptivity, not generativity, as these beliefs correspond to those endorsed within the social environment in which children are raised.

Findings from developmental psychology support the following theory of the emergence of religious belief: humans possess a suite of sophisticated cognitive adaptations for social life, which make accessible certain concepts that are associated with religion, including design, purpose, agency, and body–soul dualism. However, more is needed to generate fully-fledged, sustained, and conscious religious beliefs, including a belief in gods, in divine creation of natural entities, and in life after death. Such beliefs require cultural support.

Negativity bias and political ideology

I've just received a reviewer's copy of an upcoming article in Brain and Behavioral Science in the vein of several MindBlog posts mentioning work on the brains of conservatives versus liberals: "Differences in Negativity Bias Underlie Variations in Political Ideology" by J. R. Hibbing, K.B. Smith, and John R. Alford. I thought MindBlog readers might be interested in their abstract:

Disputes between those holding differing political views are ubiquitous, deep-seated, and often follow common, recognizable lines, with the supporters of tradition and stability, sometimes referred to as conservatives, doing battle with the supporters of innovation and reform, sometimes referred to as liberals. Understanding the correlates of these distinct political orientations is likely a prerequisite for managing political disputes, a source of social conflict often leading to frustration and even bloodshed. A rapidly growing body of empirical evidence documents a multitude of ways in which liberals and conservatives differ from each other in purviews of life with little direct connection to politics, from tastes in art to desire for closure and from disgust sensitivity to the tendency to pursue new information, but the central theme of these differences is a matter of debate. In this article, we argue that one organizing element of the many differences between liberals and conservatives is the nature of their physiological and psychological responses to features of the environment that are negative. Compared to liberals, conservatives tend to register greater physiological responses to such stimuli and also to devote more psychological resources to them. Operating from this point of departure, we suggest future approaches for refining understanding of the broad relationship between political views and response to the negative. We conclude with a discussion of normative implications, stressing that identifying differences across ideological groups is not tantamount to declaring one ideology superior to another.

Reversal of hearing decline with aging.

It is known that life-long musical experience partially offsets age-related neural timing delays. Such delays make it harder to process speech in noisy environments, and hearing aids don't help. (This is one reason I keep giving piano recitals). In a fascinating recent article, Anderson et al. show a partial reversal of these age-related neural timing delays can be partially reversed by cognitive auditory training. Edited from their text (in which the data show the indicated expectation were confirmed):

An auditory training group (n = 35) completed an adaptive computer-based auditory training program that combines bottom-up perceptual discrimination exercises with top-down cognitive demands. The second group (active control; n = 32) participated in a general educational stimulation program that was matched for time and computer use to that of the auditory training group. We recorded auditory brainstem responses to the speech syllable [da] presented in quiet and noise and assessed speech-in-noise perception, short-term memory, and speed of processing before and after 8 wk of training. We expected that auditory training would induce earlier brainstem peak latencies at posttest compared with pretest, and that the effects of noise on response timing would be reduced. Given previously demonstrated cognitive and perceptual gains from both short-term and long-term auditory training, we expected that auditory training would also improve speech-in-noise perception, short-term memory, and speed of processing.

The abstract:

Neural slowing is commonly noted in older adults, with consequences for sensory, motor, and cognitive domains. One of the deleterious effects of neural slowing is impairment of temporal resolution; older adults, therefore, have reduced ability to process the rapid events that characterize speech, especially in noisy environments. Although hearing aids provide increased audibility, they cannot compensate for deficits in auditory temporal processing. Auditory training may provide a strategy to address these deficits. To that end, we evaluated the effects of auditory-based cognitive training on the temporal precision of subcortical processing of speech in noise. After training, older adults exhibited faster neural timing and experienced gains in memory, speed of processing, and speech-in-noise perception, whereas a matched control group showed no changes. Training was also associated with decreased variability of brainstem response peaks, suggesting a decrease in temporal jitter in response to a speech signal. These results demonstrate that auditory-based cognitive training can partially restore age-related deficits in temporal processing in the brain; this plasticity in turn promotes better cognitive and perceptual skills.

By the way, on this topic, Miller has a recent interesting article on the brain basis of the "cocktail party effect', how we single out a single voice in a room full of conversations.

How to dress to say it is wrong to be gay!

I had to pass this on.....

FABULOUS! The Pope Emeritus, wearing a fabulous vintage chiffon-lined Dior gold lame gown
over a silk Vera Wang empire waist tulle cocktail dress,
accessorized with a three-foot House of Whoville hat
and the ruby slippers Judy Garland wore in the Wizard of Oz,
on his way to tell us it's wrong to be gay.

Stay plain and simple, Francis! Stay plain and simple!

Does cannabis use cause lower IQ?

Rogeberg offers a critique of a recent suggestion by Meyer et. al. of a neurotoxic effect of cannabis on developing brains that permanently lowers IQ, based on on a correlation between persistent cannabis use initiated in adolescence and a decline in IQ-scores between the ages of 13 and 38. The data come  the" Dunedin cohort," 1,037 individuals followed from birth (1972/1973) to age 38 y. An alternative confounding model can be based on time-varying effects of socioeconomic status on IQ.

Does cannabis use have substantial and permanent effects on neuropsychological functioning? Renewed and intense attention to the issue has followed recent research on the Dunedin cohort, which found a positive association between, on the one hand, adolescent-onset cannabis use and dependence and, on the other hand, a decline in IQ from childhood to adulthood [Meier et al. (2012) Proc Natl Acad Sci USA 109(40):E2657–E2664]. The association is given a causal interpretation by the authors, but existing research suggests an alternative confounding model based on time-varying effects of socioeconomic status on IQ. A simulation of the confounding model reproduces the reported associations from the Dunedin cohort, suggesting that the causal effects estimated in Meier et al. are likely to be overestimates, and that the true effect could be zero. Further analyses of the Dunedin cohort are proposed to distinguish between the competing interpretations. Although it would be too strong to say that the results have been discredited, the methodology is flawed and the causal inference drawn from the results premature.

Observing regulatory connections correlating with emotion control during transition to adolescence.

Interesting work from Gee et al. showing some brain changes that correlate with the inhibition of emotional reactivity that occurs during human adolescence:

Recent human imaging and animal studies highlight the importance of frontoamygdala circuitry in the regulation of emotional behavior and its disruption in anxiety-related disorders. Although tracing studies have suggested changes in amygdala–cortical connectivity through the adolescent period in rodents, less is known about the reciprocal connections within this circuitry across human development, when these circuits are being fine-tuned and substantial changes in emotional control are observed. The present study examined developmental changes in amygdala–prefrontal circuitry across the ages of 4–22 years using task-based functional magnetic resonance imaging. Results suggest positive amygdala–prefrontal connectivity in early childhood that switches to negative functional connectivity during the transition to adolescence. Amygdala–medial prefrontal cortex functional connectivity was significantly positive (greater than zero) among participants younger than 10 years, whereas functional connectivity was significantly negative (less than zero) among participants 10 years and older, over and above the effect of amygdala reactivity. The developmental switch in functional connectivity was paralleled by a steady decline in amygdala reactivity. Moreover, the valence switch might explain age-related improvement in task performance and a developmentally normative decline in anxiety. Initial positive connectivity followed by a valence shift to negative connectivity provides a neurobiological basis for regulatory development and may present novel insight into a more general process of developing regulatory connections.

How do alligators get errections?

I couldn't resist passing on this Discoblog pointer to Kelly's article. Most birds, reptiles, and mammals have penises that become erect by filling with fluid, but the alligator penis does not change shape or stiffness before sex. Kelly suggests it is popped out of the cloaca by muscles evolved for this purpose:

The intromittent organs of most amniotes contain variable-volume hydrostatic skeletons that are stored in a flexible state and inflate with fluid before or during copulation. However, the penis in male crocodilians is notable because its shaft does not seem to change either its shape or bending stiffness as blood enters its vascular spaces before copulation. Here I report that crocodilians may have evolved a mechanism for penile shaft erection that does not require inflation and detumescence. Dissections of the cloaca in sexually mature male American alligators (Alligator mississippiensis) show that the cross section of the proximal shaft of the alligator penis contains dense collagenous tissues that do not significantly change shape when fluid is added to the central vascular space. The large amount of collagen in the wall and central space of the alligator penis stiffen the structure so it can be simply everted for copulation and rapidly retracted at its completion. Because no muscles insert directly onto the penis, eversion and retraction must be produced indirectly. My results suggest that the contraction of paired levator cloacae muscles around the anterior end of the cloaca rotates the penis out of the cloacal opening and strains the ligamentum rami that connect the base of the penis to the ischia. When the cloacal muscles relax, the elastic recoil of the ligamentum rami can return the penis to its original position inside the cloaca.

Anti-aging drugs - Clarification on Resveratrol and SIRT1 activators

Resveratrol, the natural compound in red wine, and other small molecules are allosteric activators of SIRT1, an enzyme with roles in many biological processes (including DNA repair, metabolism, programmed cell death, and inflammation) that affect human life span. Studies have shown that Sirtuin activators like resveratrol can extend the lifespan of yeast, worms, and flies. From an editor's summary of work by Hubbard et al in the latest issue of Science:

Intense attention has focused on the SIRT1 deacetylase as a possible target for anti-aging drugs. But unexpected complications in assays of SIRT1 activity have made it unclear whether compounds thought to be sirtuin-activating compounds (STACs) are really direct regulators of the enzyme. Further exploration of these effects by Hubbard et al. revealed that interaction of SIRT1 with certain substrates allows activation of SIRT1 by STACs and identified critical amino acids in SIRT1 required for these effects. Mouse myoblasts reconstituted with SIRT1 mutated at this amino acid lost their responsiveness to STACs.

The Hubbard et al abstract:

A molecule that treats multiple age-related diseases would have a major impact on global health and economics. The SIRT1 deacetylase has drawn attention in this regard as a target for drug design. Yet controversy exists around the mechanism of sirtuin-activating compounds (STACs). We found that specific hydrophobic motifs found in SIRT1 substrates such as PGC-1α and FOXO3a facilitate SIRT1 activation by STACs. A single amino acid in SIRT1, Glu230, located in a structured N-terminal domain, was critical for activation by all previously reported STAC scaffolds and a new class of chemically distinct activators. In primary cells reconstituted with activation-defective SIRT1, the metabolic effects of STACs were blocked. Thus, SIRT1 can be directly activated through an allosteric mechanism common to chemically diverse STACs.

The mental cost of cognitive enhancement.

There has been quite a bit of interest lately in the prospect of enhancing various brain operations by the use of trans-cranial electrical stimulation (TES). Iuculano and Kadosh make the fascinating observation that enhancing one activity with TES can compromise another:

Noninvasive brain stimulation provides a potential tool for affecting brain functions in the typical and atypical brain and offers in several cases an alternative to pharmaceutical intervention. Some studies have suggested that transcranial electrical stimulation (TES), a form of noninvasive brain stimulation, can also be used to enhance cognitive performance. Critically, research so far has primarily focused on optimizing protocols for effective stimulation, or assessing potential physical side effects of TES while neglecting the possibility of cognitive side effects. We assessed this possibility by targeting the high-level cognitive abilities of learning and automaticity in the mathematical domain. Notably, learning and automaticity represent critical abilities for potential cognitive enhancement in typical and atypical populations. Over 6 d, healthy human adults underwent cognitive training on a new numerical notation while receiving TES to the posterior parietal cortex or the dorsolateral prefrontal cortex. Stimulation to the the posterior parietal cortex facilitated numerical learning, whereas automaticity for the learned material was impaired. In contrast, stimulation to the dorsolateral prefrontal cortex impaired the learning process, whereas automaticity for the learned material was enhanced. The observed double dissociation indicates that cognitive enhancement through TES can occur at the expense of other cognitive functions. These findings have important implications for the future use of enhancement technologies for neurointervention and performance improvement in healthy populations.

And you thought you knew the data on wealth inequality?

I found this a jaw-dropping clarification of wealth inequality in the U.S.

Can the Catholic Church evolve?

Maureen Dowd discusses gay author Colin Toibin’s “The Testament of Mary,” a one-woman show with Fiona Shaw previewing later this month on Broadway, and I pass on this fascinating clip on Toibin’s thoughts about the Church and homosexuality (I was fascinated to learn about Benedict's “Gorgeous Georg”, who he takes with him into retirement.):

Benedict may have given up his flashy red loafers, downgrading to brown ones made for him in Mexico, but he is taking “Gorgeous Georg,” as the younger German is known, to live in his new home, a monastery in the Vatican. Some cardinals are worried about the arrangement of having Gänswein serve two pontiffs, by day as prefect of the new pope’s household and at night as secretary to the emeritus pope.

“An 85-year-old man having such a beautiful companion with him morning and night to talk to and walk with,” Toibin said. “It’s like the end of a novel. It’s what all of us want for ourselves, straight or gay. It’s better than sex.”

I ask him whether he thinks the church will evolve under a new pope.

“Everyone is hoping for some change,” he said. “If you could see nuns making sermons. Clerical celibacy has to be abolished and soon. And we must quickly begin the process of allowing women into the priesthood.

“They need to think very carefully about not recognizing that gay people, like all other people, are made in God’s image. It’s just possible that they have more gay priests than they know. I think most gay priests are very good people in the priesthood for very good reasons, and actually faithful to the vows of celibacy. On the issue of gays, Benedict made things even worse.”

As Cardinal Ratzinger, Benedict called homosexuality a “more or less strong tendency ordered towards an intrinsic moral evil.” As pope, he reiterated the church view that homosexuals were “objectively disordered” and that men who had such tendencies could not be allowed into seminaries. He called gay marriage a threat to “the future of humanity itself.”

Toibin says that the church must have tolerance, and that its leaders have lost any sense of how their sanctimonious denunciations clash with their scandals and imagery, causing nothing but pain.

“I remember being at the Vatican at Easter 1994,” he recalled, “and watching all the cardinals and bishops, wonderfully powerful old men with great chins, sitting nobly with a long row of extraordinarily beautiful young seminarians standing behind, shading them with different colored sun umbrellas, some of which were pink."

“It was remarkable that none of them seemed to know what it looked like, and I watched it thinking, somebody must tell them.”

Neural mechanisms of stress vulnerability and resilience.

Two interesting papers in the Journal of Neuroscience  deal with what is happening to nerve cells in mouse brains as they either do or don't recover from stress. Lehmann et al. demonstrate that glucocorticoid-dependent declines in neurogenesis drive changes in mood after social defeat and that glucocorticoids secreted during enrichment promote hippocampal neurogenesis and restore normal behavior after defeat, suggesting that treatments promoting neurogenesis can enhance stress resilience. Gourley et al. looked at the elimination of dendritic spines in the hippocampus caused by chronic stress exposure, and show that resilience, or recovery from stress, correlates with spine proliferation.

In praise of the unexamined, unlived life?

I was sufficiently interested by two reviews of a new book by British psychoanalyst Adam Phillips (“Missing Out: In Praise of the Unlived Life”), one in the NYTimes (Sheila Heti), one in The New Yorker (Joan Acocella), that I downloaded a Kindle version to look over. I totally regret having spent the 11 bucks. There are two main messages noted by reviewers, one is the dressing up of homily common to many self help books. From Acocella:

Instead of feeling that we should have a better life, he says, we should just live, as gratifyingly as possible, the life we have.  Otherwise, we are setting ourselves up for bitterness.  What makes us think that we could have been a contender?  Yet, in the dark of night, we do think this, and grieve that it wasn’t possible.  “And what was not possible all too easily becomes the story of our lives,” Phillips writes.  “Out lived lives might become a protracted mourning for, or an endless trauma about, the lives we were unable to live.”

OK, fair enough. It can be an error to spend our  time thinking on what we might have been or want to be or ought to be or be doing, rather than just living  and being who we are, getting on with it.  Just doing things. The rub is that Phillips is completely unwilling to write simple sentences with simple ideas. He generates complex elliptical sentences designed more to illustrate his erudition and mental pyrotechnics than to inform, lost in a world of abstraction.

I completely lost it with his second chapter "On Not Getting It," where he essentially argues that we are better off not understanding ourselves, or others. His correct contention that we can never really understand ourselves or others is beside the point. Our illusions of understanding ourselves and others are a feature evolved by our social brains that has proven its utility in enhancing and passing on the genes of groups of humans who share common illusions. And, we sure have gotten a lot of mileage out of trying to understand. Otherwise we wouldn't be attempting to read psychoanalytic babble like Philips' or write things like MindBlogs.

Is the insula necessary for our feelings? If not, where are they?

I have been fairly uncritical in passing on simplifications like “The insula is the sensory cortex for our internal visceral feelings” and so was grateful to see, in Damasio’s recent review article “The nature of feelings: evolutionary and neurobiological origins” a critique of this idea:

Feelings and the insula. Interoceptive information mapped in the brainstem is projected rostrally to the subcortical basal forebrain and to the cortical telencephalon, where it is remapped in the insula and somatosensory cortices SI and SII.

Contemporary neuroscience has identified the insula as the main cortical target for signals from the interoceptive system, and functional neuroimaging studies consistently implicate the human insula in both interoceptive and emotional feelings.

Recently, it has been proposed that the insula is not merely involved in human feelings but is their sole platform and, by extension, the critical provider of human awareness. Several findings suggest that this hypothesis is problematic. First, given that several topographically organized nuclei of the upper brainstem, which are obligatory relay stations for most signals conveyed from the body to the insula, can produce elaborate representations of multiple parameters of body states, these regions should not be excluded a priori as platforms for feelings. Second, children born without cerebral cortex exhibit behaviours compatible with feeling states. Third, bilateral insular damage does not abolish all feelings. Specifically, complete bilateral destruction of the insula as a result of herpes simplex encephalitis does not abolish either body or emotional feelings, including pain, pleasure, itch, tickle, happiness, sadness, apprehension, irritation, caring and compassion, in addition to hunger, thirst, and bladder and colon distension. In fact, feelings seem to dominate the mental landscape of patients with bilateral insular damage. Immediate comfort appears to be their main concern, fairly unbridled by cognitive constraints.

These observations do not support a view of the insula as a necessary substrate for feeling states. Thus, the generation of feelings must also rely on the brainstem and possibly on the SI and SII somatosensory cortices of the parietal lobe, which are spared in some patients that lack the insular cortices but remain fully capable of feeling. Indeed, damage to the posterior half of the upper brainstem is associated with coma or vegetative state — two conditions in which feelings and sentience are abolished.

After reviewing data on how feelings persist after lesions to other cortical regions suggested central to feelings, Damasio suggests that subcortical regions such as the upper brainstem and hypothalamus are most central in the generation of feelings, and that this has resounding evolutionary implications:

...the fundamental elements of body state mapping, sentience and feelings imbued with valence are likely to be far older than our species, and probably even older than the advent of cerebral cortices. There is good reason to believe that the primate brain inherited the neural instruments for feeling from its ancestors and elaborated upon them.

Watching our auditory brain, like a radio, switch hearing frequency channels.

From Da Costa et al.:

Cocktail parties, busy streets, and other noisy environments pose a difficult challenge to the auditory system: how to focus attention on selected sounds while ignoring others? Neurons of primary auditory cortex, many of which are sharply tuned to sound frequency, could help solve this problem by filtering selected sound information based on frequency-content. To investigate whether this occurs, we used high-resolution fMRI at 7 tesla to map the fine-scale frequency-tuning (1.5 mm isotropic resolution) of primary auditory areas A1 and R in six human participants. Then, in a selective attention experiment, participants heard low (250 Hz)- and high (4000 Hz)-frequency streams of tones presented at the same time (dual-stream) and were instructed to focus attention onto one stream versus the other, switching back and forth every 30 s. Attention to low-frequency tones enhanced neural responses within low-frequency-tuned voxels relative to high, and when attention switched the pattern quickly reversed. Thus, like a radio, human primary auditory cortex is able to tune into attended frequency channels and can switch channels on demand.

Amygdala damage can make us more generous

From van Honk et al.:

Contemporary economic models hold that instrumental and impulsive behaviors underlie human social decision making. The amygdala is assumed to be involved in social-economic behavior, but its role in human behavior is poorly understood. Rodent research suggests that the basolateral amygdala (BLA) subserves instrumental behaviors and regulates the central-medial amygdala, which subserves impulsive behaviors. The human amygdala, however, typically is investigated as a single unit. If these rodent data could be translated to humans, selective dysfunction of the human BLA might constrain instrumental social-economic decisions and result in more impulsive social-economic choice behavior. Here we show that humans with selective BLA damage and a functional central-medial amygdala invest nearly 100% more money in unfamiliar others in a trust game than do healthy controls. We furthermore show that this generosity is not caused by risk-taking deviations in nonsocial contexts. Moreover, these BLA-damaged subjects do not expect higher returns or perceive people as more trustworthy, implying that their generous investments are not instrumental in nature. These findings suggest that the human BLA is essential for instrumental behaviors in social-economic interactions.

Here is the anatomical location of the human lesions:

MR images (coronal view) of the three subjects with Urbach–Wiethe disease (UWD), with their year of birth and red crosshairs indicating the calcified brain damage...the lesions of the three patients are located in the BLA...the functional method shows activation during emotion matching in the superficial amygdala (SFA) and CMA, but not in the BLA.

How our viscera influence our brain and behavior

I want to pass on this fascinating and useful open source review by Critchley and Harrison in the journal Neuron. Having just had the flu, I found their presentation of visceral regulation of sickness behaviors very relevant! The article is worthwhile especially for the summary figures showing functional and anatomical pathways. (I resist the urge to paste them into this post, you can look at them by clicking on the link above. Here is their abstract:

Mental processes and their neural substrates are intimately linked to the homeostatic control of internal bodily state. There are a set of distinct interoceptive pathways that directly and indirectly influence brain functions. The anatomical organization of these pathways and the psychological/behavioral expressions of their influence appear along discrete, evolutionarily conserved dimensions that are tractable to a mechanistic understanding. Here, we review the role of these pathways as sources of biases to perception, cognition, emotion, and behavior and arguably the dynamic basis to the concept of self.

And, two clips from the text:

The internal state of the body motivates our desire to walk in the shade on a warm summer’s day and inhibits the desire to eat or socialize when feeling off-color. Communication from the viscera to brain is continuous and pervasive, yet we rarely give it a second thought. Visceral fluctuations and reactions accessible to introspective appraisal represent only the visible tip of the iceberg.

A comprehensive understanding of the integration of internal bodily signals in health is ultimately required for effective management of physical and psychological symptoms in illness. Such a goal can only be achieved through coordinated experimental approaches and perhaps a move away from treating physiological changes as irrelevant confounds in neuropsychological experiments. Together, these observations make “us realize more deeply than ever how much of our mental life is knit up in our corporeal frame” (James, 1890).

How ambient light might influence our mood.

The visual pigment melanopsin in the intrinsically photosensitive retinal ganglion cells (ipRGCs) of our inner retinas (two cells layers away from our rods and cones) detect ambient light and send this information to brain areas that regulate circadian rhythms and mood. LaGates et al. have now found that inappropriately timed light exposure that does not alter normal sleep architecture and circadian rhythmicity of body temperature and general activity still can cause impaired learning and depression-like behaviors in mice. In mice genetically altered to remove ipRGC cells, the depressive-like behaviors and learning deficits are not observed. If similar mechanisms operate in us humans, this suggests a potential mechanism by which abnormal ambient light schedules — caused by shift work or simply switching on an artificial light — might influence mood and learning. Here is their abstract:

The daily solar cycle allows organisms to synchronize their circadian rhythms and sleep–wake cycles to the correct temporal niche. Changes in day-length, shift-work, and transmeridian travel lead to mood alterations and cognitive function deficits. Sleep deprivation and circadian disruption underlie mood and cognitive disorders associated with irregular light schedules. Whether irregular light schedules directly affect mood and cognitive functions in the context of normal sleep and circadian rhythms remains unclear. Here we show, using an aberrant light cycle that neither changes the amount and architecture of sleep nor causes changes in the circadian timing system, that light directly regulates mood-related behaviours and cognitive functions in mice. Animals exposed to the aberrant light cycle maintain daily corticosterone rhythms, but the overall levels of corticosterone are increased. Despite normal circadian and sleep structures, these animals show increased depression-like behaviours and impaired hippocampal long-term potentiation and learning. Administration of the antidepressant drugs fluoxetine or desipramine restores learning in mice exposed to the aberrant light cycle, suggesting that the mood deficit precedes the learning impairments. To determine the retinal circuits underlying this impairment of mood and learning, we examined the behavioural consequences of this light cycle in animals that lack intrinsically photosensitive retinal ganglion cells. In these animals, the aberrant light cycle does not impair mood and learning, despite the presence of the conventional retinal ganglion cells and the ability of these animals to detect light for image formation. These findings demonstrate the ability of light to influence cognitive and mood functions directly through intrinsically photosensitive retinal ganglion cells.

The lament of the historian…

My colleague William Cronon at the University of Wisconsin was President of the American Historical Association for 2012,  and I want to pass on a clip from the AHA Presidential Address he delivered in Jan. 2013.  Among his concerns about the future of historical studies as a discipline is the digital revolution and internet that are transforming literally everything about the way historians work and how people read:

One of my deepest fears about this brave new digital world has to do with reading itself...It seems to me that the book-length monograph on which our discipline has long relied is very much at risk as texts migrate from paper to screens. It is not just that libraries are reducing purchases, that university presses are facing cutbacks, or that declining print runs and rising per-unit costs are pricing many specialized monographs beyond the reach of ordinary buyers. My deeper fear comes from watching my own students, many of whom no longer read books for pleasure. If they have any prior experience doing research, almost all of it is online. If a piece of information cannot be Googled, it effectively does not exist for them. More than a few of my students have never actually been inside the stacks of a library. To the extent that good writing is predicated on frequent skilled reading, the ability of such students to recognize and construct grammatical sentences and paragraphs—let alone graceful or elegant ones—is plummeting.

In a manically multitasking world where even e-mail takes too long to read, where texts and tweets and Facebook postings have become dominant forms of communication, reading itself is more at risk than many of us realize. Or, to be more precise, long-form reading is at risk: the ability to concentrate and sustain one's attention on arguments and narratives for many hours and many thousands of words. I have come to think of this as the Anna Karenina problem: will students twenty years from now be able to read novels like Tolstoy's that are among the greatest works of world literature but that require dozens of hours to be meaningfully experienced? And if a novel as potent as Anna lies beyond reach, what does that imply for complex historical monographs that are in many ways even more challenging in the demands they make on readers?

What is the future of history?...there is one answer that is arguably the most basic of all, and that is, simply: storytelling. We need to remember the roots of our discipline and be sure to keep telling stories that matter as much to our students and to the public as they do to us. Although the shape and form of our stories will surely change to meet the expectations of this digital age, the human need for storytelling is not likely ever to go away. It is far too basic to the way people make sense of their lives—and among the most important stories they tell are those that seek to understand the past. Hang on to this truth, and there is no reason to fear that history will be any less important to the human future than it has been to the human past.

In an uncertain world, fairness finishes first.

I usually get hopelessly lost in accounts of variations of the ultimatum game used to model human behavior and its evolutionary rationale or origins. This experiment by Rand et al. seems relatively clear and crisp:

Classical economic models assume that people are fully rational and selfish, while experiments often point to different conclusions. A canonical example is the Ultimatum Game: one player proposes a division of a sum of money between herself and a second player, who either accepts or rejects. Based on rational self-interest, responders should accept any nonzero offer and proposers should offer the smallest possible amount. Traditional, deterministic models of evolutionary game theory agree: in the one-shot anonymous Ultimatum Game, natural selection favors low offers and demands. Experiments instead show a preference for fairness: often responders reject low offers and proposers make higher offers than needed to avoid rejection. Here we show that using stochastic evolutionary game theory, where agents make mistakes when judging the payoffs and strategies of others, natural selection favors fairness. Across a range of parameters, the average strategy matches the observed behavior: proposers offer between 30% and 50%, and responders demand between 25% and 40%. Rejecting low offers increases relative payoff in pairwise competition between two strategies and is favored when selection is sufficiently weak. Offering more than you demand increases payoff when many strategies are present simultaneously and is favored when mutation is sufficiently high. We also perform a behavioral experiment and find empirical support for these theoretical findings: uncertainty about the success of others is associated with higher demands and offers; and inconsistency in the behavior of others is associated with higher offers but not predictive of demands. In an uncertain world, fairness finishes first.