ScienceBlogs Channel : Brain & Behavior

Casual Fridays: What makes a good writer? [Cognitive Daily]

Dave Munger none@example.com — Fri, 13 Nov 2009 16:51:24 -0500

Some people just seem to be natural writers -- they can write perfect, elegant sentences with a minimum of effort. Some popular fiction novelists crank out 6 or more novels per year. Some bloggers write 10 or more posts per day. Others labor over every word, or simply choose careers that don't require a lot of writing. But are there universal characteristics that separate good writers from bad writers, and quick writers from slow writers?

I think I may have come up with a quick study that can answer those questions -- and like all Casual Fridays studies, it can be completed in just a few minutes. With any luck, we may have some (non-scientific) insight into what makes a good writer -- or at least a quick one.

Click here to participate

As usual, the study is brief, with about 15 questions. It should take only a few minutes to complete. You have until Thursday, November 19 to complete your response. There is no limit on the number of respondents. Don't forget to come back next week for the results!

(Just a reminder: All Casual Fridays studies are non-scientific. This doesn't mean we can't use scientific principles to assess what's going on, but we can't make general claims based on the results)

Read the comments on this post...

Dopamine and Future Forecasting [The Frontal Cortex]

Jonah Lehrer none@example.com — Fri, 13 Nov 2009 11:20:36 -0500

Ed Yong has a typically excellent post on a new paper that looks at how manipulating dopamine levels in the brain can change our predictions of future pleasure:

Tali Sharot from University College London found that if volunteers had more dopamine in their brains as they thought about events in their future, they would imagine those events to be more gratifying. It's the first direct evidence that dopamine influences how happy we expect ourselves to be.
Sharot recruited 61 volunteers and asked them to say how happy they'd feel if they visited one of 80 holiday destinations, from Greece to Thailand. All of the recruits were given a vitamin C supplement as a placebo and 40 minutes later, they had to imagine themselves on holiday at half of the possible locations. After this bout of fanciful daydreaming, they had to take another pill but this time, half of them were given L-DOPA instead of the placebo. Again, they had to imagine themselves in various holiday spots.

The next day, Sharot brought the volunteers back. By this time, they would have broken down all the L-DOPA in their system. She asked them to choose which of two destinations they'd like to go to, from the set that they had thought about the day before. Finally, they rated each destination again.

By the end of the experiments, they perceived their imaginary holidays to be more enjoyable if they had previously thought about the locations under the influence of L-DOPA (while vitamin C, as predicted, had no effect). The implication is clear: think about the future with more dopamine in the noggin and you'll imagine that you have a better time.

As I've noted before, the popular caricature of dopamine - it's the hedonistic molecule in the brain, activated by sex, drugs and rock and roll - is slightly misleading. Dopamine neurons, it turns out, don't care about pleasure per se - they're much more interested in predicting pleasure, and then comparing our predictions to the actual event. The transactions of dopamine are largely about learning - finding a way to maximize our rewards - and not about mere decadence.

What I find so interesting about this experiment is that it neatly confirmed this theory of computational neuroscience. After all, the subjects didn't feel happier after popping a pill of L-DOPA - boosting dopamine levels didn't lead to instant gratification, like Huxley's soma. Instead, it merely altered their predictions of future happiness.

But here's the funny thing about those predictions: they tend to correlate pretty accurately with our actual experience. If you think you're going to have a good time on vacation, then you probably will, just as we tend to enjoy foods and beverages and products that we expect to enjoy. (This is the consumer version of the placebo effect.) Here's how I described similar phenomena in How We Decide:

Baba Shiv, a neuroeconomist at Stanford, supplied a group of people with Sobe Adrenaline Rush, an "energy" drink that was supposed to make them feel more alert and energetic. (The drink contained a potent brew of sugar and caffeine which, the bottle promised, would impart "superior functionality"). Some participants paid full price for the drinks, while others were offered a discount. The participants were then asked to solve a series of word puzzles. Shiv found that people who paid discounted prices consistently solved about thirty percent fewer puzzles than the people who paid full price for the drinks. The subjects were convinced that the stuff on sale was much less potent, even though all the drinks were identical. "We ran the study again and again, not sure if what we got had happened by chance or fluke," Shiv says. "But every time we ran it we got the same results."
Why did the cheaper energy drink prove less effective? According to Shiv, consumers typically suffer from a version of the placebo effect. Since we expect cheaper goods to be less effective, they generally are less effective, even if they are identical to more expensive products. This is why brand-name aspirin works better than generic aspirin, or why Coke tastes better than cheaper colas, even if most consumers can't tell the difference in blind taste tests. "We have these general beliefs about the world⎯for example, that cheaper products are of lower quality⎯and they translate into specific expectations about specific products," said Shiv. "Then, once these expectations are activated, they start to really impact our behavior.

So the next time you buy something on sale, pop a pill of L-DOPA. It will increase your pleasure, if only because you expect it to.

Read the comments on this post...

Dyslexia and the Cocktail Party effect [Neurophilosophy]

Mo none@example.com — Fri, 13 Nov 2009 11:10:23 -0500

IMAGINE sitting in a noisy restaurant, across the table from a friend, having a conversation as you eat your meal. To communicate effectively in this situation, you have to extract the relevant information from the noise in the background, as well as from other voices. To do so, your brain somehow "tags" the predictable, repeating elements of the target signal, such as the pitch of your friend's voice, and segregates them from other signals in the surroundings, which fluctuate randomly.

The ability to focus on your friend's voice while excluding other noises is commonly referred to as the cocktail party effect. Although first described more than 50 years ago, the brain mechanisms involved are unknown. But a new study by researchers at Northwestern University now shows that activity in regions of the brainstem are modulated by specific characteristics of the speaker's voice, and that this modulation is impaired in children with dyslexia.

Read the rest of this post... | Read the comments on this post...

A bit of insight about transgender and gender dysphoria [The World's Fair]

David Ng none@example.com — Fri, 13 Nov 2009 11:00:50 -0500

Alex does a great job here on this topic. This would also, I suspect, take a lot of guts to do which is both inspiring and commendable.

(If you want to leave a comment about the talk, please do so here). - - -

Topic: Alex discusses the influence of gender in his own life in this TEDx talk, describing both medical and social perspectives of gender in our daily lives and the impact and consequences these perspectives bring to every individual.

Links:
Transgender Health Program, VCH, TEDxTt09

Filmed by Craig Ross at TEDx Terry talks 2009 (October 3rd, 2009). Video edited by David Ng. See more TEDx Terry talks videos here.

Read the comments on this post...

Friday Weird Science: Oxytocin and the Big O [Neurotopia]

Scicurious none@example.com — Fri, 13 Nov 2009 00:18:00 -0500

Rounding out Sci's first week of the Great Oxytocin Posting of 2009 (oh yes, there will be two weeks of this, hang tight), we've gotta do something weird. And luckily for everyone, oxytocin does lend itself to the strange types of studies. Like multi-orgasmic studies. Complete with measurements of anal contraction. You know you wanna volunteer for this one.

And luckily for all of you, Sci is the one doing the reading and the retelling of this study. Because reading the methods for this one might cause you to do this:

(Sci reading the methods)

Carmichael et al. "Relationships among cardiovascular, muscular, and oxytocin responses during human sexual activity". Archives of Sexual Behavior, 1994.

Read the rest of this post... | Read the comments on this post...

The long-term effects of day care [Cognitive Daily]

Dave Munger none@example.com — Thu, 12 Nov 2009 17:31:41 -0500

When we were getting ready to have our first child, I decided that I would quit my job, work out of home as a freelancer, and take care of our baby while Greta finished graduate school.

That worked well for about two years, but by the time Nora was born, we decided to hire a part-time nanny so I could finish a degree of my own. When Nora was one and Greta and I were starting new jobs in a new state, both kids entered full-time day care, and that was our child-care arrangement until they started kindergarten.

Naturally, at every step along the way, we wondered whether we were making the right parenting decisions. We liked their nanny and their day-care center, but wouldn't it be better for the kids to be cared for full-time by their own parents? At that time, there wasn't a whole lot of research pointing one way or another. The definitive child-care study can probably never be done: Families would have to be randomly assigned to day-care centers or parent care for years, and then the impact of the assignments wouldn't be known until the children reached adulthood. Even then, you wouldn't know if the effects were due to particular parenting or day-care practices, or to the day-care versus parent-care assignment.

Realistically, the next best thing you can do is to follow children from birth to adulthood, and see if kids who happened to have been placed in day care (or with nannies, or grandparents, or some other arrangement) ended up better- or worse-off than those cared for by their mothers. Indeed, such a study was launched by the National Institute of Child Health and Development in the early 1990s. The results have been gradually trickling in as the children in the study aged. The most recent installment, published in 2007, covers kids through the sixth grade.

The study follows over 1,000 children who were randomly selected on their day of birth from ten U.S. hospitals. Researchers checked in intermittently with the families over the next dozen years, assessing both their family situation and the child care provided. Then when the kids entered school, they tracked their progress, got teacher reports on their social behavior, and continued to monitor the quality of their parenting (in addition to whether the kids were in after-school care programs).

Read the rest of this post... | Read the comments on this post...

Travels with dopamine - the chemical that affects how much pleasure we expect [Not Exactly Rocket Science]

Ed Yong none@example.com — Thu, 12 Nov 2009 12:00:40 -0500

How would you fancy a holiday to Greece or Thailand? Would you like to buy an iPhone or a new pair of shoes? Would you be keen to accept that enticing job offer? Our lives are riddled with choices that force us to imagine our future state of mind. The decisions we make hinge upon this act of time travel and a new study suggests that our mental simulations of our future happiness are strongly affected by the chemical dopamine.

Dopamine is a neurotransmitter, a chemical that carries signals within the brain. Among its many duties is a crucial role in signalling the feelings of enjoyment we get out of life's pleasures. We need it to learn which experiences are rewarding and to actively seek them out. And it seems that we also depend on it when we imagine the future.

Tali Sharot from University College London found that if volunteers had more dopamine in their brains as they thought about events in their future, they would imagine those events to be more gratifying. It's the first direct evidence that dopamine influences how happy we expect ourselves to be.

When we learn about new experiences, neurons that secrete dopamine seem to record the difference between the rewards we expect and the ones we actually receive. In encoding the gap between hope and experience, these neurons help us to repeat rewarding actions.

This was clearly demonstrated in 2006, when Mathias Passiglione showed that people's ability to learn about rewards could be improved by giving them a drug called L-DOPA. It's a precursor to dopamine, a sort of parent molecule that can increase the concentrations of its offspring. Passiglione asked volunteers to learn links between different symbols and different financial rewards. He found that under the influence of L-DOPA, they were better at picking the symbols that earned them the most cash.

Passiglione's study was important, but his volunteers were forced to make a fairly artificial choice between two virtual symbols in a constrained lab setting. What happens in real life, when choices are complex and our decisions hinge on our ability to think about the future?

To answer that, Sharot recruited 61 volunteers and asked them to say how happy they'd feel if they visited one of 80 holiday destinations, from Greece to Thailand. All of the recruits were given a vitamin C supplement as a placebo and 40 minutes later, they had to imagine themselves on holiday at half of the possible locations. After this bout of fanciful daydreaming, they had to take another pill but this time, half of them were given L-DOPA instead of the placebo. Again, they had to imagine themselves in various holiday spots.

The next day, Sharot brought the volunteers back. By this time, they would have broken down all the L-DOPA in their system. She asked them to choose which of two destinations they'd like to go to, from the set that they had thought about the day before. Finally, they rated each destination again.

By the end of the experiments, they perceived their imaginary holidays to be more enjoyable if they had previously thought about the locations under the influence of L-DOPA (while vitamin C, as predicted, had no effect). The implication is clear: think about the future with more dopamine in the noggin and you'll imagine that you have a better time.

Critically, this wasn't because they were feeling happier in the actual moment. All the recruits filled in questionnaires about their emotional state every time they took a pill and these revealed that the dopamine boost didn't actually affect the present state of mind. All it did was change their predictions of their future state of mind. These happier predictions affected their choices too - more often than not, they chose to travel to destinations that they had envisioned through dopamine-tinted goggles.

How dopamine has its way is unclear. Sharot suggests that it could boost how much we want something when we imagine it. Its effects could also tie into its role in learning. When we imagine the future, this chemical strengthens the link between what we think about and any feelings of enjoyment we might gain from it. This model fits with the fact that some neurons in the striatum become more active the more pleasure we expect from an experience.

Either way, it's clear that our knowledge of dopamine's myriad roles is just beginning. Broadening that knowledge is important for understanding our own behaviour, which, as Sharot says, "is largely driven by estimations of future pleasure and pain".

Reference: Current Biology 10.1016/j.cub.2009.10.025

More on Sharot's work and dopamine:

Read the rest of this post... | Read the comments on this post...

Senator Asks Pentagon To Review Antidepressants [Neuron Culture]

David Dobbs none@example.com — Thu, 12 Nov 2009 11:36:12 -0500

Ben Cardin, a Maryland Democrat, has asked the Pentagon for info on how many troops in war zones have been prescribed antidepressants while they were deployed. Cardin sent a letter Tuesday to US Department of Defense Secretary Robert Gates expressing concern about how antidepressants are being administered troops in Iraq and Afghanistan.

Cardin wants to determine if the Defense Department is prescribing antidepressants appropriately and is concerned about any connection between the meds and suicide rates among troops. In October, for instance, 16 active-duty US soldiers killed themselves, bringing the total number of active-duty suicides in 2009 to 134. At this rate, the number of 2009 suicides will eclipse last year's total of 140 - the highest yearly number of suicides in Army history. Cardin also notes the rate of active-duty suicides is greater than that of the US population, although he doesn't question the "long-term efficacy" of the drugs.

via pharmalot.com

Most soldier/vet suicides get blamed on PTSD. This overlooks a couple important things:

1. Depression and drinking problems are both more common than PTSD is, even among combat vets, and have a more robustly established and higher suicide risk.

2. As the story above notes, antidepressant use among younger people, especially if not monitored closely, is shown to carry a significant suicide risk.

Cardin's effort is an attempt to address the second problem. This is a good example of how reflexive diagnoses, as PTSD has become for any combat veteran (and sometimes even prospective combat veterans -- i.e., troops preparing to deploy), can do harm. They can lead you to ignore other possible causes of the symptoms on display.

Posted via web from David Dobbs's Somatic Marker

Read the comments on this post...

Raymond Tallis trashtalks some "Neurotrash" [Neuron Culture]

David Dobbs none@example.com — Thu, 12 Nov 2009 10:03:36 -0500

Hardly a day passes without yet another breathless declaration in the popular press about the relevance of neuroscientific findings to everyday life. The articles are usually accompanied by a picture of a brain scan in pixel-busting Technicolor and are frequently connected to references to new disciplines with the prefix "neuro-". Neuro-jurisprudence, neuro-economics, neuro-aesthetics, neuro-theology are encroaching on what was previously the preserve of the humanities. Even philosophers - who should know better, being trained one hopes, in scepticism - have entered the field with the discipline of "Exp-phi" or experimental philosophy. Starry-eyed sages have embraced "neuro-ethics", in which ethical principles are examined by using brain scans to determine people's moral intuitions when they are asked to deliberate on the classic dilemmas. Benjamin Libet's experiments on decisions to act and the work on mirror neurons (observed directly in monkeys but only inferred, and still contested, in humans) have been ludicrously over-interpreted to demonstrate respectively that our brains call the shots (and we do not have free will) and to point to a neural basis for empathy.

via newhumanist.org.uk

Ray Tallis talks trash to neurotrash who talk too much neuro. Suggested read; good for all your neuromatter.

Posted via web from David Dobbs's Somatic Marker

Read the comments on this post...

Revisiting FOXP2 and the origins of language [Not Exactly Rocket Science]

Ed Yong none@example.com — Wed, 11 Nov 2009 13:00:40 -0500

Today, a new paper published in Nature adds another chapter to the story of FOXP2, a gene with important roles in speech and language. The FOXP2 story is a fascinating tale that I covered in New Scientist last year. It's one of the pieces I'm proudest of so I'm reprinting it here with kind permission from Roger Highfield, and with edits incorporating new discoveries since the time of writing.

The FOXP2 Story (2009 edition)

Imagine an orchestra full of eager musicians which, thanks to an incompetent conductor, produces nothing more than an unrelieved cacophony. You're starting to appreciate the problem faced by a British family known as KE. About half of its members have severe difficulties with language. They have trouble with grammar, writing and comprehension, but above all they find it hard to coordinate the complex sequences of face and mouth movements necessary for fluid speech.

Thanks to a single genetic mutation, the conductor cannot conduct, and the result is linguistic chaos. In 2001, geneticists looking for the root of the problem tracked it down to a mutation in a gene they named FOXP2. Normally, FOXP2 coordinates the expression of other genes, but in affected members of the KE family, it was broken.

It had long been suspected that language has some basis in genetics, but this was the first time that a specific gene had been implicated in a speech and language disorder. Overeager journalists quickly dubbed FOXP2 "the language gene" or the "grammar gene". Noting that complex language is a characteristically human trait, some even speculated that FOXP2 might account for our unique position in the animal kingdom. Scientists were less gushing but equally excited - the discovery sparked a frenzy of research aiming to uncover the gene's role.

Several years on, and it is clear that talk of a "language gene" was premature and simplistic. Nevertheless, FOXP2 tells an intriguing story. "When we were first looking for the gene, people were saying that it would be specific to humans since it was involved in language," recalls Simon Fisher at the University of Oxford, who was part of the team that identified FOXP2 in the KE family. In fact, the gene evolved before the dinosaurs and is still found in many animals today: species from birds to bats to bees have their own versions, many of which are remarkably similar to ours. "It gives us a really important lesson," says Fisher. "Speech and language didn't just pop up out of nowhere. They're built on very highly conserved and evolutionarily ancient pathways."

Two amino acids, two hundred thousand years

The first team to compare FOXP2 in different species was led by Wolfgang Enard from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. In 2001, they looked at the protein that FOXP2 codes for, called FOXP2, and found that our version differs from those of chimpanzees, gorillas and rhesus macaques by two amino acids out of a total of 715, and from that of mice by three. This means that the human version of FOXP2 evolved recently and rapidly: only one amino acid changed in the 130 million years since the mouse lineage split from that of primates, but we have picked up two further differences since we diverged from chimps, and this seems to have happened only with the evolution of our own species at most 200,000 years ago.

The similarity between the human protein FOXP2 and that of other mammals puts it among the top 5 per cent of the most conserved of all our proteins. What's more, different human populations show virtually no variation in their FOXP2 gene sequences. Last year, Enard's colleague Svante Pääbo made the discovery that Neanderthals also had an identical gene, prompting questions over their linguistic abilities (see "Neanderthal echoes below).

"People sometimes think that the mutated FOXP2 in the KE family is a throwback to the chimpanzee version, but that's not the case," says Fisher. The KEs have the characteristically human form of the gene. Their mutation affects a part of the FOXP2 protein that interacts with DNA, which explains why it has trouble orchestrating the activity of other genes.

There must have been some evolutionary advantage associated with the human form of FOXP2, otherwise the two mutations would not have spread so quickly and comprehensively through the population. What this advantage was, and how it may have related to the rise of language, is more difficult to say. Nevertheless, clues are starting to emerge as we get a better picture of what FOXP2 does - not just in humans but in other animals too.

During development, the gene is expressed in the lungs, oesophagus and heart, but what interests language researchers is its role in the brain. Here there is remarkable similarity across species: from humans to finches to crocodiles, FOXP2 is active in the same regions. With no shortage of animal models to work with, several teams have chosen songbirds due to the similarities between their songs and human language: both build complex sequences from basic components such as syllables and riffs, and both forms of vocalisation are learned through imitation and practice during critical windows of development.

Babbling birds

All bird species have very similar versions of FOXP2. In the zebra finch, its protein is 98 per cent identical to ours, differing by just eight amino acids. It is particularly active in a part of the basal ganglia dubbed "area X", which is involved in song learning. Constance Scharff at the Max Planck Institute for Molecular Genetics in Berlin, Germany, reported that finches' levels of FOXP2 expression in area X are highest during early life, which is when most of their song learning takes place. In canaries, which learn songs throughout their lives, levels of the protein shoot up annually and peak during the late summer months, which happens to be when they remodel their songs.

So what would happen to a bird's songs if levels of the FOXP2 protein in its area X were to plummet during a crucial learning window? Scharff found out by injecting young finches with a tailored piece of RNA that inhibited the expression of the FOXP2 gene. The birds had difficulties in developing new tunes and their songs became garbled: they contained the same component "syllables" as the tunes of their tutors, but with syllables rearranged, left out, repeated incorrectly or sung at the wrong pitch.

The cacophony produced by these finches bears uncanny similarities to the distorted speech of the afflicted KE family members, making it tempting to pigeonhole FOXP2 as a vocal learning gene - influencing the ability to learn new communication sounds by imitating others. But that is no more accurate than calling it a "language gene". For a start, songbird FOXP2 has no characteristic differences to the gene in non-songbirds. What's more, among other species that show vocal learning, such as whales, dolphins and elephants, there are no characteristic patterns of mutation in their FOXP2 that they all share.

Instead, consensus is emerging that FOXP2 probably plays a more fundamental role in the brain. Its presence in the basal ganglia and cerebellums of different animals provides a clue as to what that role might be. Both regions help to produce precise sequences of muscle movements. Not only that, they are also able to integrate information coming in from the senses with motor commands sent from other parts of the brain. Such basic sensory-motor coordination would be vital for both birdsong and human speech. So could this be the key to understanding FOXP2?

Moving mice

New work by Fisher and his colleagues supports this idea. In 2008, his team engineered mice to carry the same FOXP2 mutation that affects the KE family, rendering the protein useless. Mice with two copies of the dysfunctional FOXP2 had shortened lives, characterised by motor disorders, growth problems and small cerebellums. Mice with one normal copy of FOXP2 and one faulty copy (as is the case in the affected members of the KE family) seemed outwardly healthy and capable of vocalisation, but had subtle defects.

For example, they found it difficult to acquire new motor skills such as learning to run faster on a tilted running wheel. An examination of their brains revealed the problem. The synapses connecting neurons within the cerebellum, and those in a part of the basal ganglia called the striatum in particular, were severely flawed. The signals that crossed these synapses failed to develop the long-term changes that are crucial for memory and learning. The opposite happened when the team engineered mice to produce a version of FOXP2 with the two characteristically human mutations. Their basal ganglia had neurons with longer outgrowths (dendrites) that were better able to strengthen or weaken the connections between them.

A battery of over 300 physical and mental tests showed that the altered mice were generally healthy. While they couldn't speak like their cartoon equals, their central nervous system developed in different ways, and they showed changes in parts of the brain where FOXP2 is usually expressed (switched on) in humans.

Their squeaks were also subtly transformed. When mouse babies are moved away from their nest, they make ultrasonic distress calls that are too high for us to hear, but that their mothers pick up loudly and clearly. The altered Foxp2 gene subtly changed the structure of these alarm calls. We won't know what this means until we get a better understanding of the similarities between mouse calls and human speech.

For now, the two groups of engineered mice tentatively support the idea that human-specific changes to FOXP2 affect aspects of speech, and strongly support the idea that they affect aspects of learning. "This shows, for the first time, that the [human-specific] amino-acid changes do indeed have functional effects, and that they are particularly relevant to the brain," explains Fisher. "FOXP2 may have some deeply conserved role in neural circuits involved in learning and producing complex patterns of movement." He suspects that mutant versions of FOXP2 disrupt these circuits and cause different problems in different species.

Pääbo agrees. "Language defects may be where problems with motor coordination show up most clearly in humans, since articulation is the most complex set of movements we make in our daily life," he says. These circuits could underpin the origins of human speech, creating a biological platform for the evolution of both vocal learning in animals and spoken language in humans.

Holy diversity, Batman

The link between FOXP2 and sensory-motor coordination is bolstered further by research in bats. Sequencing the gene in 13 species of bats, Shuyi Zhang and colleagues from the East China Normal University in Shanghai discovered that it shows incredible diversity. Why would bats have such variable forms of FOXP2 when it is normally so unwavering in other species?

Zhang suspects that the answer lies in echolocation. He notes that the different versions seem to correspond with different systems of sonar navigation used by the various bat species. Although other mammals that use echolocation, such as whales and dolphins, do not have special versions of FOXP2, he points out that since they emit their sonar through their foreheads, these navigation systems have fewer moving parts. Furthermore, they need far less sensory-motor coordination than flying bats, which vocalise their ultrasonic pulses and adjust their flight every few milliseconds, based on their interpretation of the echoes they receive.

These bats suggest that FOXP2 is no more specific to basic communication than it is to language, and findings from other species tell a similar tale. Nevertheless, the discovery that this is an ancient gene that has assumed a variety of roles does nothing to diminish the importance of its latest incarnation in humans.

Since its discovery, no other gene has been convincingly implicated in overt language disorders. FOXP2 remains our only solid lead into the genetics of language. "It's a molecular window into those kinds of pathways - but just one of a whole range of different genes that might be involved," says Fisher. "It's a starting point for us, but it's not the whole story." He has already used FOXP2 to hunt down other key players in language.

The executive's minions

FOXP2 is a transcription factor, which activates some genes while suppressing others. Identifying its targets, particularly in the human brain, is the next obvious step. Working with Daniel Geschwind at the University of California, Los Angeles, Fisher has been trying to do just that, and their preliminary results indicate just what a massive job lies ahead. On their first foray alone, the team looked at about 5000 different genes and found that FOXP2 potentially regulates hundreds of these.

Some of these target genes control brain development in embryos and its continuing function in adults. Some affect the structural pattern of the developing brain and the growth of neurons. Others are involved in chemical signalling and the long-term changes in neural connections that enable to learning and adaptive behaviour. Some of the targets are of particular interest, including 47 genes that are expressed differently in human and chimpanzee brains, and a slightly overlapping set of 14 targets that have evolved particularly rapidly in humans.

Most intriguingly, Fisher says, "we have evidence that some FOXP2 targets are also implicated in language impairment." Last year, Sonja Vernes in his group showed that FOXP2 switches off CNTNAP2, a gene involved in not one but two language disorders - specific language impairment (SLI) and autism. Both affect children, and both involve difficulties in picking up spoken language skills. The protein encoded by CNTNAP2 is deployed by nerve cells in the developing brain. It affects the connections between these cells and is particularly abundant in neural circuits that are involved in language.

Verne's discovery is a sign that the true promise of FOXP2's discovery is being fulfilled - the gene itself has been overly hyped, but its true worth lies in opening a door for more research into genes involved in language. It was the valuable clue that threw the case wide open. CNTNAP2 may be the first language disorder culprit revealed through FOXP2 and it's unlikely to be the last.

Most recently, Dan Geschwind compared the network of genes that are targeted by FOXP2 in both chimps and humans. He found that the two human-specific amino acids within this executive protein have radically altered the set of genetic minions that it controls.

The genes that are directed by human FOXP2 are a varied cast of players that influence the development of the head and face, parts of the brain involved in motor skills, the growth of cartilage and connective tissues, and the development of the nervous system. All those roles fit with the idea that our version of FOXP2 has been a lynchpin in evolving the neural circuits and physical structures that are important for speech and language.

The FOXP2 story is far from complete, and every new discovery raises fresh questions just as it answers old ones. Already, this gene has already taught us important lessons about evolution and our place in the natural world. It shows that our much vaunted linguistic skills are more the result of genetic redeployment than out-and-out innovation. It seems that a quest to understand how we stand apart from other animals is instead leading to a deeper appreciation of what unites us.

Box - Neanderthal echoes

The unique human version of the FOXP2 gives us a surprising link with one extinct species. Last year, Svante Pääbo's group at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from the bones of two Neanderthals, one of the first instances of geneticists exploring ancient skeletons for specific genes. They found that Neanderthal FOXP2 carries the same two mutations as those carried by us - mutations accrued since our lineage split from chimps between 6 and 5 million years ago.

Pääbo admits that he "struggled" to interpret the finding: the Neanderthal DNA suggests that the modern human's version of FOXP2 arose much earlier than previously thought. Comparisons of gene sequences of modern humans with other living species had put the origins of human FOXP2 between 200,000 and 100,000 years ago, which matches archaeological estimates for the emergence of spoken language. However, Neanderthals split with humans around 400,000 years ago, so the discovery that they share our version of FOXP2 pushes the date of its emergence back at least that far.
"We believe there were two things that happened in the evolution of human FOXP2," says Pääbo. "The two amino acid changes - which happened before the Neanderthal-human split - and some other change which we don't know about that caused the selective sweep more recently." In other words, the characteristic mutations that we see in human FOXP2 may indeed be more ancient than expected, but the mutated gene only became widespread and uniform later in human history. While many have interpreted Pääbo's findings as evidence that Neanderthals could talk, he is more cautious. "There's no reason to assume that they weren't capable of spoken language, but there must be many other genes involved in speech that we yet don't know about in Neanderthals."

Read the rest of this post... | Read the comments on this post...

Deep brain stimulation for clinical depression? [Cognitive Daily]

Dave Munger none@example.com — Wed, 11 Nov 2009 11:49:20 -0500

This week on SEED, I'm writing about Deep Brain Stimulation (DBS), a promising new way to treat clinical depression. Here's a snippet:

In DBS therapy, one or more electrodes the size of a spaghetti strand are precisely positioned in the patient's brain, then connected by wire around the skull and through the neck to a pacemaker-like device, a neurostimulator, just below the collarbone. The neurostimulator is activated and deactivated by a magnet that the patient carries, so if a tremor is beginning to become disruptive, DBS can be self-administered in an instant, with near-instantaneous results. A video provided by the manufacturer of a DBS device shows how it works in ideal cases.
Now new uses for the treatment are being tested. One observed side effect of DBS for Parkinson's is excessive happiness, to the point of uncontrollable elation--the sort of unhealthy, personality-changing reaction that everyone fears when they think of electrodes being implanted in their brain. Tuning the device can minimize this side effect, but its very existence suggests that DBS might be a useful therapy for clinical depression.

For more, read the whole article.

Also, in case you missed it, here are my picks for psychology and neuroscience from ResearchBlogging.org:

Can you tell how strong someone is just by looking at their face? Michael Meadon looks at research suggesting that you can.
What does your genome say about how likely you are to go into debt? Quite a lot, says the Neurocritic.
Think you've finally got control over your weight? Now's about the time you'll probably start putting those pounds back on.
How do you make a non-threatening area seem unsafe? Just put a closed-circuit surveillance camera there.

Read the comments on this post...

Inside of a Dog by Alexandra Horowitz [Uncertain Principles]

Chad Orzel none@example.com — Wed, 11 Nov 2009 09:58:04 -0500

I've gradually gotten used to the idea that as a semi-pro blogger, I will occasionally be sent review copies of books I've never heard of. These are generally physics books, and I have a stack of them sitting next to the bed at the moment, not being read nearly fast enough.

It's only recently that I realized that, having written a book in which I explain quantum mechanics through conversations with my dog, I'll probably start getting dog books as well. Not that there's anything wrong with that, mind-- we like free books, here in Chateau Steelypips-- but it's going to be a significant change.

Inside of a Dog: What Dogs See, Smell, and Know is not, strictly speaking, an unsolicited review copy-- it's also a Scribner book, and my editor sent it to me. Because, well, it's a science book about dogs. The author, Alexandra Horowitz, is a cognitive scientist at Columbia, and the book is based around both her experiences as a scientist studying dogs, and her experiences as a pet owner. It mixes small vignettes of life with her dog:

This morning I was awakened by Pump coming over to the bed and sniffing emphatically at me, millimeters away, her whiskers grazing my lips, to see if I was awake or alive or me. She punctuates her rousing with an exclamatory sneeze directly in my face. I open my eyes and she is gazing at me, smiling, panting a hello.

with more scientifically oriented material:

Read the rest of this post... | Read the comments on this post...

New and Exciting in PLoS ONE [A Blog Around The Clock]

Coturnix none@example.com — Wed, 11 Nov 2009 08:31:37 -0500

There are 23 new articles in PLoS ONE today. As always, you should rate the articles, post notes and comments and send trackbacks when you blog about the papers. You can now also easily place articles on various social services (CiteULike, Mendeley, Connotea, Stumbleupon, Facebook and Digg) with just one click. Here are my own picks for the week - you go and look for your own favourites:

Biomechanics of Running Indicates Endothermy in Bipedal Dinosaurs:

One of the great unresolved controversies in paleobiology is whether extinct dinosaurs were endothermic, ectothermic, or some combination thereof, and when endothermy first evolved in the lineage leading to birds. Although it is well established that high, sustained growth rates and, presumably, high activity levels are ancestral for dinosaurs and pterosaurs (clade Ornithodira), other independent lines of evidence for high metabolic rates, locomotor costs, or endothermy are needed. For example, some studies have suggested that, because large dinosaurs may have been homeothermic due to their size alone and could have had heat loss problems, ectothermy would be a more plausible metabolic strategy for such animals. Here we describe two new biomechanical approaches for reconstructing the metabolic rate of 14 extinct bipedal dinosauriforms during walking and running. These methods, well validated for extant animals, indicate that during walking and slow running the metabolic rate of at least the larger extinct dinosaurs exceeded the maximum aerobic capabilities of modern ectotherms, falling instead within the range of modern birds and mammals. Estimated metabolic rates for smaller dinosaurs are more ambiguous, but generally approach or exceed the ectotherm boundary. Our results support the hypothesis that endothermy was widespread in at least larger non-avian dinosaurs. It was plausibly ancestral for all dinosauriforms (perhaps Ornithodira), but this is perhaps more strongly indicated by high growth rates than by locomotor costs. The polarity of the evolution of endothermy indicates that rapid growth, insulation, erect postures, and perhaps aerobic power predated advanced "avian" lung structure and high locomotor costs.

Foreign Subtitles Help but Native-Language Subtitles Harm Foreign Speech Perception:

Understanding foreign speech is difficult, in part because of unusual mappings between sounds and words. It is known that listeners in their native language can use lexical knowledge (about how words ought to sound) to learn how to interpret unusual speech-sounds. We therefore investigated whether subtitles, which provide lexical information, support perceptual learning about foreign speech. Dutch participants, unfamiliar with Scottish and Australian regional accents of English, watched Scottish or Australian English videos with Dutch, English or no subtitles, and then repeated audio fragments of both accents. Repetition of novel fragments was worse after Dutch-subtitle exposure but better after English-subtitle exposure. Native-language subtitles appear to create lexical interference, but foreign-language subtitles assist speech learning by indicating which words (and hence sounds) are being spoken.

Egg Eviction Imposes a Recoverable Cost of Virulence in Chicks of a Brood Parasite:

Chicks of virulent brood parasitic birds eliminate their nestmates and avoid costly competition for foster parental care. Yet, efforts to evict nest contents by the blind and naked common cuckoo Cuculus canorus hatchling are counterintuitive as both adult parasites and large older cuckoo chicks appear to be better suited to tossing the eggs and young of the foster parents. Here we show experimentally that egg tossing imposed a recoverable growth cost of mass gain in common cuckoo chicks during the nestling period in nests of great reed warbler Acrocephalus arundinaceus hosts. Growth rates of skeletal traits and morphological variables involved in the solicitation of foster parental care remained similar between evictor and non-evictor chicks throughout development. We also detected no increase in predation rates for evicting nests, suggesting that egg tossing behavior by common cuckoo hatchlings does not increase the conspicuousness of nests. The temporary growth cost of egg eviction by common cuckoo hatchlings is the result of constraints imposed by rejecter host adults and competitive nestmates on the timing and mechanism of parasite virulence.

Beyond Word Frequency: Bursts, Lulls, and Scaling in the Temporal Distributions of Words:

Zipf's discovery that word frequency distributions obey a power law established parallels between biological and physical processes, and language, laying the groundwork for a complex systems perspective on human communication. More recent research has also identified scaling regularities in the dynamics underlying the successive occurrences of events, suggesting the possibility of similar findings for language as well. By considering frequent words in USENET discussion groups and in disparate databases where the language has different levels of formality, here we show that the distributions of distances between successive occurrences of the same word display bursty deviations from a Poisson process and are well characterized by a stretched exponential (Weibull) scaling. The extent of this deviation depends strongly on semantic type - a measure of the logicality of each word - and less strongly on frequency. We develop a generative model of this behavior that fully determines the dynamics of word usage. Recurrence patterns of words are well described by a stretched exponential distribution of recurrence times, an empirical scaling that cannot be anticipated from Zipf's law. Because the use of words provides a uniquely precise and powerful lens on human thought and activity, our findings also have implications for other overt manifestations of collective human dynamics.

Read the comments on this post...

Oxytocin: This one's for the Ladies [Neurotopia]

Scicurious none@example.com — Wed, 11 Nov 2009 00:58:10 -0500

Previously I posted on the general features of oxytocin, what it acts on, and where it basically acts, and what it's mostly known for. But the reality is that oxytocin is a LOT more complicated than that, and has different effects of your body and your behavior, depending on who you are. It varies from person to person (as all biological things do) as well as between men and women. And today, we're going to discuss the ladies. Because if there is anything oxytocin is famous for, it's for its effects on women.

(Yes, yes, we will cover this bit).

You may have noticed lots of links in the previous post. Those links are to the literature which I searched before posting. There will be lots more links in this one to examples of studies which support what I'm going to tell you about. Of course, all of these are in science-ese, and so if you are puzzling over something and can't make it out, give a shout out in the comments with the particular paper, and Sci will do her best to cover the paper later on. I have a feeling that oxytocin is going to be a recurring topic.

So here we go.

This one's for the ladies

Read the rest of this post... | Read the comments on this post...

Do chimps understand what Jon Stewart (or another chimp) believes? [Cognitive Daily]

Dave Munger none@example.com — Tue, 10 Nov 2009 17:09:04 -0500

Take a look at this video from last night's episode of Jon Stewart's "The Daily Show."

If you'd like, you can skip past all the political snark to the 4:47 mark to watch Jon bring cognitive psychology into prime time (or at least latenight cable)! That's right; you saw it: Jon Stewart mentioned the psychological concept of "object permanence" on national TV. Object permanence was introduced by Jean Piaget as a way of measuring the growing cognitive ability of children. Three-month-olds don't have it; most 6-month-olds do. More recently, researchers have investigated similar milestones in animals. Parrots, it turns out, have object permanence, as do chimpanzees. Insects don't.

But what about higher-order cognitive functions? Do chimps understand that others have thoughts distinct from their own? Humans understand this around the age of 1, but the evidence is less clear with chimps. Some chimps will use gestures alone to beg for food from a blindfolded human. Does this mean they don't "know" the human can't see them? Perhaps not, but normally a chimp doesn't expect to communicate with a human. When two chimps are in two separate rooms, but can see into a third room where food is being hidden, the subordinate chimp will behave differently if she knows the dominant chimp saw the food being hidden. This suggests chimps do understand that other chimps have different thoughts from their own.

Read the rest of this post... | Read the comments on this post...

Orchid Genes [The Frontal Cortex]

Jonah Lehrer none@example.com — Tue, 10 Nov 2009 15:28:42 -0500

David Dobbs has a fantastic new article on behavioral genetics at The Atlantic. He adds an important amendment to the vulnerability hypothesis, which holds that certain genes make people more vulnerable to psychiatric disorders. While these snippets of DNA aren't deterministic per se, when they are combined with traumatic childhood events, or a stressful few months, they can lead to serious mental illness. It's the old genes plus environment story, and it's typically cast in a negative light. But Dobbs finds that the vulnerability hypothesis comes with a positive (and often overlooked) flip-side:

At first glance, this idea, which I'll call the orchid hypothesis, may seem a simple amendment to the vulnerability hypothesis. It merely adds that environment and experience can steer a person up instead of down. Yet it's actually a completely new way to think about genetics and human behavior. Risk becomes possibility; vulnerability becomes plasticity and responsiveness. It's one of those simple ideas with big, spreading implications. Gene variants generally considered misfortunes (poor Jim, he got the "bad" gene) can instead now be understood as highly leveraged evolutionary bets, with both high risks and high potential rewards: gambles that help create a diversified-portfolio approach to survival, with selection favoring parents who happen to invest in both dandelions and orchids.
In this view, having both dandelion and orchid kids greatly raises a family's (and a species') chance of succeeding, over time and in any given environment. The behavioral diversity provided by these two different types of temperament also supplies precisely what a smart, strong species needs if it is to spread across and dominate a changing world. The many dandelions in a population provide an underlying stability. The less-numerous orchids, meanwhile, may falter in some environments but can excel in those that suit them. And even when they lead troubled early lives, some of the resulting heightened responses to adversity that can be problematic in everyday life--increased novelty-seeking, restlessness of attention, elevated risk-taking, or aggression--can prove advantageous in certain challenging situations: wars, tribal or modern; social strife of many kinds; and migrations to new environments. Together, the steady dandelions and the mercurial orchids offer an adaptive flexibility that neither can provide alone. Together, they open a path to otherwise unreachable individual and collective achievements.

This orchid hypothesis also answers a fundamental evolutionary question that the vulnerability hypothesis cannot. If variants of certain genes create mainly dysfunction and trouble, how have they survived natural selection? Genes so maladaptive should have been selected out. Yet about a quarter of all human beings carry the best-documented gene variant for depression, while more than a fifth carry the variant that Bakermans-Kranenburg studied, which is associated with externalizing, antisocial, and violent behaviors, as well as ADHD, anxiety, and depression. The vulnerability hypothesis can't account for this. The orchid hypothesis can.

This is a transformative, even startling view of human frailty and strength. For more than a decade, proponents of the vulnerability hypothesis have argued that certain gene variants underlie some of humankind's most grievous problems: despair, alienation, cruelties both petty and epic. The orchid hypothesis accepts that proposition. But it adds, tantalizingly, that these same troublesome genes play a critical role in our species' astounding success.

The orchid hypothesis--sometimes called the plasticity hypothesis, the sensitivity hypothesis, or the differential-susceptibility hypothesis--is too new to have been tested widely. Many researchers, even those in behavioral science, know little or nothing of the idea. A few--chiefly those with broad reservations about ever tying specific genes to specific behaviors--express concerns. But as more supporting evidence emerges, the most common reaction to the idea among researchers and clinicians is excitement. A growing number of psychologists, psychiatrists, child-development experts, geneticists, ethologists, and others are beginning to believe that, as Karlen Lyons-Ruth, a developmental psychologist at Harvard Medical School, puts it, "It's time to take this seriously."

Read the comments on this post...

People who think they are more restrained are more likely to succumb to temptation [Not Exactly Rocket Science]

Ed Yong none@example.com — Tue, 10 Nov 2009 09:30:30 -0500

Will you have that extra chocolate bar when you're worried about your weight? Will you spend that extra hour on the internet when you have other things to do? Will you have that extra drink with an attractive colleague when your partner is waiting at home? Our lives are full of temptations and some of us are better at resisting them than others. But unexpectedly, the very people who think they are most restrained are also most likely to be impulsive. Their inflated belief in their own self-control leads them to overexpose themselves to temptation.

In a series of four experiments, Loran Nordgren from Northwestern University showed that people suffer from a "restraint bias", where they overestimate their ability to control their own impulses. Those who fall prey to this fallacy most strongly are more likely to dive into tempting situations. Smokers, for example, who are trying to quit, are more likely to put themselves in situations if they think they're invulnerable to temptation. As a result, they're more likely to relapse.

The restraint bias stems from the fact that we're generally bad at predicting the future and how we'd feel in circumstances that are different to our current ones. When we're full, we underestimate the powerful pangs of hunger. When we're cold, we can't imagine what it's really like to be sweltering. Addicts underestimate the pull of their drug-of choice when they try to quit.

Nordgren showed this in a previous experiment, where he asked people to remember how much dunking their hand in an icy bucket would affect their performance in a memory test. He found that people underestimated the memory-killing power of the ice, unless they were actually doing it at the time.

This time, he wanted to see how this restraint bias actually affects our behaviour. He started by asking 72 students to memorise strings of numbers for either an easy 2 minutes or a strenuous, tiring 20 minutes. As expected, those who did the longer task felt more tired than those who did the shorter one. They also felt that they had less control over their mental fatigue and they were less likely to cram for their final exams, leaving significantly less of their studying until the last week. This confirms that, like the case of the icy bucket, students overestimate their ability to fight off tiredness unless they're actually experiencing it, and this affects how they plan their studying.

In another study, Nordgren asked 79 people to rank seven snacks in order of preference, either as they entered or left a cafeteria. He also asked them to pick one of the snacks and said that they would win it, and four euros, if they returned it uneaten a week later (the snacks were tagged to avoid cheats).

He found that people leaving the cafeteria were not only less hungry than those entering it, they also felt more strongly about their ability to shrug off an impulsive craving for snacks. That came through in their choices - the full volunteers generally chose one of their two favourite snacks, while the hungry ones chose their second- or third-favourite. On an individual basis, people who thought more of their impulse control were more likely to choose the more tempting snack. They were also less likely to actually return with the snack.

For his final studies, Nordgren wanted to actually manipulate his volunteers' belief in their resistance to temptation. He gave 53 smokers a test that would tell them if they had a low or high capacity for controlling their impulses. The test, however, was a sham and it's decrees were random. Nonetheless, those who were told they had lots of control were more likely to believe it than those who were assigned to the low-control group.

After being manipulated, the volunteers played a self-control game where could win money by watching a film Coffee and Cigarettes without lighting up. They could choose their difficulty setting - they could either watch the film with a cigarette in another room, on their desk, in their hand, or in their mouth (unlit, of course). The harder the challenge, the greater the potential prize.

As you've probably guessed by now, smokers who were told they had more control exposed themselves to the more tempting scenarios (they typically opted for the cigarette in hand, while the other preferred it on the table). However, their self-beliefs didn't pan out - they were three times more likely to actually smoke the cigarettes than their peers, despite being allegedly less impulsive.

This fits with other studies which have found that smokers underestimate the cravings they'll face when they try to quit. And after cravings cease, self-delusion becomes even greater. Nordgren interviewed 55 people who had quit smoking for three weeks and found that those who were most confident about their impulse-control were more likely to put themselves in tempting situations. They were less likely to ask people to not smoke around them, and more likely to hang around other smokers, keep cigarettes around them and think that they could have an occasional cigarette without truly relapsing. And the price of this confidence? They were more likely to relapse after four months.

Together, Nordgren's four studies beautifully demonstrate the power of the restraint bias in real-life settings. It's a phenomenon that has powerful consequences, especially when it affects behaviours like smoking or dietary choices that could have significant effects on people's health. It also applies to several situations where temptation rears its head. Should a married person knowingly go for dinner with an attractive ex, on the assumption that they'll resist their attraction? Should a busy professional buy a time-sucking computer game based on their confidence that they'll manage their time effectively?

The restraint bias could also help to explain why people willingly take up activities they already know to be addictive - they simply believe that they're strong enough to resist the addiction. As a powerful example of this, one study showed that heroin users are less willing to pay for the substitute buprenorphine if they weren't currently experiencing cravings. If experienced users underestimate their urges, imagine how monumentally more difficult it would be for a naive person to do so.

This study, like many others I've reported on, speaks to the massive importance of self-awareness. Unrealistic perceptions of ourselves can wreak havoc with our decision making. Overinflated views of ourselves give us further to fall when our status is challenged. If we think we're more controlled than we are, we're more likely to lose control. If we say unrealistically positive things about ourselves, we could actually damage our self-esteem.

It's no coincidence that many addiction programs encourage people to have a more realistic sense of themselves. Alcoholic Anonymous, for example, emphasises that alcoholics should admit that they are powerless over alcohol and that they will always remain an alcoholic. Nordgren says that these recurring themes could help people to avoid "[drifting] back toward the illusory belief that they can handle their cravings."

Reference:

More unexpected psychology:

Read the rest of this post... | Read the comments on this post...

New and Exciting in PLoS this week [A Blog Around The Clock]

Coturnix none@example.com — Tue, 10 Nov 2009 09:07:35 -0500

Let's take a look at recent papers in PLoS ONE and other PLoS journals. As always, you should rate the articles, post notes and comments and send trackbacks when you blog about the papers. You can now also easily place articles on various social services (CiteULike, Mendeley, Connotea, Stumbleupon, Facebook and Digg) with just one click. Here are my own picks for the week - you go and look for your own favourites:

Chemically-Mediated Roostmate Recognition and Roost Selection by Brazilian Free-Tailed Bats (Tadarida brasiliensis):

The Brazilian free-tailed bat (Tadarida brasiliensis) is an exceptionally social and gregarious species of chiropteran known to roost in assemblages that can number in the millions. Chemical recognition of roostmates within these assemblages has not been extensively studied despite the fact that an ability to chemically recognize individuals could play an important role in forming and stabilizing complex suites of social interactions. Individual bats were given a choice between three roosting pouches: one permeated with the scent of a group of roostmates, one permeated with the scent of non-roostmates, and a clean control. Subjects rejected non-roostmate pouches with greater frequency than roostmate pouches or blank control pouches. Also, bats chose to roost in the roostmate scented pouches more often than the non-roostmate or control pouches. We demonstrated that T. brasiliensis has the ability to chemically recognize roostmates from non-roostmates and a preference for roosting in areas occupied by roostmates. It is important to investigate these behaviors because of their potential importance in colony dynamics and roost choice.

Phospholipase C-β4 Is Essential for the Progression of the Normal Sleep Sequence and Ultradian Body Temperature Rhythms in Mice:

The sleep sequence: i) non-REM sleep, ii) REM sleep, and iii) wakefulness, is stable and widely preserved in mammals, but the underlying mechanisms are unknown. It has been shown that this sequence is disrupted by sudden REM sleep onset during active wakefulness (i.e., narcolepsy) in orexin-deficient mutant animals. Phospholipase C (PLC) mediates the signaling of numerous metabotropic receptors, including orexin receptors. Among the several PLC subtypes, the β4 subtype is uniquely localized in the geniculate nucleus of thalamus which is hypothesized to have a critical role in the transition and maintenance of sleep stages. In fact, we have reported irregular theta wave frequency during REM sleep in PLC-β4-deficient mutant (PLC-β4−/−) mice. Daily behavioral phenotypes and metabotropic receptors involved have not been analyzed in detail in PLC-β4−/− mice, however. Therefore, we analyzed 24-h sleep electroencephalogram in PLC-β4−/− mice. PLC-β4−/− mice exhibited normal non-REM sleep both during the day and nighttime. PLC-β4−/− mice, however, exhibited increased REM sleep during the night, their active period. Also, their sleep was fragmented with unusual wake-to-REM sleep transitions, both during the day and nighttime. In addition, PLC-β4−/− mice reduced ultradian body temperature rhythms and elevated body temperatures during the daytime, but had normal homeothermal response to acute shifts in ambient temperatures (22°C-4°C). Within the most likely brain areas to produce these behavioral phenotypes, we found that, not orexin, but group-1 metabotropic glutamate receptor (mGluR)-mediated Ca2+ mobilization was significantly reduced in the dorsal lateral geniculate nucleus (LGNd) of PLC-β4−/− mice. Voltage clamp recordings revealed that group-1 mGluR-mediated currents in LGNd relay neurons (inward in wild-type mice) were outward in PLC-β4−/− mice. These lines of evidence indicate that impaired LGNd relay, possibly mediated via group-1 mGluR, may underlie irregular sleep sequences and ultradian body temperature rhythms in PLC-β4−/− mice.

Rat Merkel Cells Are Mechanoreceptors and Osmoreceptors:

Merkel cells (MCs) associated with nerve terminals constitute MC-neurite complexes, which are involved in slowly-adapting type I mechanoreception. Although MCs are known to express voltage-gated Ca2+ channels and hypotonic-induced membrane deformation is known to lead to Ca2+ transients, whether MCs initiate mechanotransduction is currently unknown. To answer to this question, rat MCs were transfected with a reporter vector, which enabled their identification. Their properties were investigated through electrophysiological studies. Voltage-gated K+, Ca2+ and Ca2+-activated K+ (KCa) channels were identified, as previously described. Here, we also report the activation of Ca2+ channels by histamine and their inhibition by acetylcholine. As a major finding, we demonstrated that direct mechanical stimulations induced strong inward Ca2+ currents in MCs. Depolarizations were dependent on the strength and the length of the stimulation. Moreover, touch-evoked currents were inhibited by the stretch channel antagonist gadolinium. These data confirm the mechanotransduction capabilities of MCs. Furthermore, we found that activation of the osmoreceptor TRPV4 in FM1-43-labeled MCs provoked neurosecretory granule exocytosis. Since FM1-43 blocks mechanosensory channels, this suggests that hypo-osmolarity activates MCs in the absence of mechanotransduction. Thus, mechanotransduction and osmoreception are likely distinct pathways.

Dynamics of the Leaf-Litter Arthropod Fauna Following Fire in a Neotropical Woodland Savanna:

Fire is an important agent of disturbance in tropical savannas, but relatively few studies have analyzed how soil-and-litter dwelling arthropods respond to fire disturbance despite the critical role these organisms play in nutrient cycling and other biogeochemical processes. Following the incursion of a fire into a woodland savanna ecological reserve in Central Brazil, we monitored the dynamics of litter-arthropod populations for nearly two years in one burned and one unburned area of the reserve. We also performed a reciprocal transplant experiment to determine the effects of fire and litter type on the dynamics of litter colonization by arthropods. Overall arthropod abundance, the abundance of individual taxa, the richness of taxonomic groups, and the species richness of individual taxa (Formiciade) were lower in the burned site. However, both the ordinal-level composition of the litter arthropod fauna and the species-level composition of the litter ant fauna were not dramatically different in the burned and unburned sites. There is evidence that seasonality of rainfall interacts with fire, as differences in arthropod abundance and diversity were more pronounced in the dry than in the wet season. For many taxa the differences in abundance between burned and unburned sites were maintained even when controlling for litter availability and quality. In contrast, differences in abundance for Collembola, Formicidae, and Thysanoptera were only detected in the unmanipulated samples, which had a lower amount of litter in the burned than in the unburned site throughout most of our study period. Together these results suggest that arthropod density declines in fire-disturbed areas as a result of direct mortality, diminished resources (i.e., reduced litter cover) and less favorable microclimate (i.e., increased litter desiccation due to reduction in tree cover). Although these effects were transitory, there is evidence that the increasingly prevalent fire return interval of only 1-2 years may jeopardize the long-term conservation of litter arthropod communities.

University Public-Access Mandates Are Good for Science:

Why would university faculty choose to place their scholarship on electronic archives for a world-wide audience? Many US universities have adopted such mandates for public access to faculty research, perhaps most notably Harvard [1], MIT, and the University of Kansas [2]. These policies (and many more like them in various stages of consideration on campuses across the nation and world) are harbingers of a new order, one in which essentially all scholarly articles can be found and accessed by any interested individual.

Read the comments on this post...

I'm not vulnerable, just especially plastic. Risk genes, environment, and evolution, in the Atlantic [Neuron Culture]

David Dobbs none@example.com — Tue, 10 Nov 2009 08:15:02 -0500

The video interview above, with NIH primatologist Stephen Suomi, is embedded within a feature of mine that that appeared today at The Atlantic website -- and is in the December 2009 issue now shipping -- about a new hypothesis in behavioral genetics.

This emerging hypothesis, which draws on substantial data, much of which has gone simply unnoticed or unremarked, I call the "orchid-gene hypothesis," for lack of a better name. Some of the researchers have other offerings. It's been around for several years but is now blooming as evidence accumulates. When I came across it at a conference this spring -- gaggles of scientists talking excitedly in the halls -- it immediately struck me as a deeply transformative and powerful idea. It recasts the genes we now see simply as 'risk alleles' for things such as depression or ADHD as 'sensitivity' genes that create greater responsiveness not just to bad environments (creating the well-documented risk) but good environments -- creating an upside to these genes that has gone largely unnoticed.

It is thus

a new interpretation of one of the most important and influential ideas in recent psychiatric and personality research: that certain variants of key behavioral genes (most of which affect either brain development or the processing of the brain's chemical messengers) make people more vulnerable to certain mood, psychiatric, or personality disorders. Bolstered over the past 15 years by numerous studies, this hypothesis, often called the "stress diathesis" or "genetic vulnerability" model, has come to saturate psychiatry and behavioral science. During that time, researchers have identified a dozen-odd gene variants that can increase a person's susceptibility to depression, anxiety, attention-deficit hyperactivity disorder, heightened risk-taking, and antisocial, sociopathic, or violent behaviors, and other problems--if, and only if, the person carrying the variant suffers a traumatic or stressful childhood or faces particularly trying experiences later in life.
This vulnerability hypothesis, as we can call it, has already changed our conception of many psychic and behavioral problems. It casts them as products not of nature or nurture but of complex "gene-environment interactions." Your genes don't doom you to these disorders. But if you have "bad" versions of certain genes and life treats you ill, you're more prone to them.

Recently, however, an alternate hypothesis has emerged from this one and is turning it inside out. This new model suggests that it's a mistake to understand these "risk" genes only as liabilities. Yes, this new thinking goes, these bad genes can create dysfunction in unfavorable contexts--but they can also enhance function in favorable contexts. The genetic sensitivities to negative experience that the vulnerability hypothesis has identified, it follows, are just the downside of a bigger phenomenon: a heightened genetic sensitivity to all experience.
Read the rest of this post... | Read the comments on this post...

Smell and Memory [The Frontal Cortex]

Jonah Lehrer none@example.com — Mon, 09 Nov 2009 11:01:17 -0500

A new paper by scientists at the Weizmann Institute documents the primal connection between whiffs of smell and episodic memory. This nasal nostalgia is mediated by the hippocampus, the manufacturer of long-term memory in the brain. Here's the abstract:

Authors, poets, and scientists have been fascinated by the strength of childhood olfactory memories. Indeed, in long-term memory, the first odor-to-object association was stronger than subsequent associations of the same odor with other objects. Here we tested the hypothesis that first odor associations enjoy a privileged brain representation. Because emotion impacts memory, we further asked whether the pleasantness of an odor would influence such a representation. On day 1, we associated the same visual objects initially with one, and subsequently with a second, set of pleasant and unpleasant olfactory and auditory stimuli. One week later, we presented the same visual objects and tested odor-associative memory concurrent with functional magnetic resonance brain imaging. We found that the power (% remembered) of early associations was enhanced when they were unpleasant, regardless of whether they were olfactory or auditory. Brain imaging, however, revealed a unique hippocampal activation for early olfactory but not auditory associations, regardless of whether they were pleasant or unpleasant. Activity within the hippocampus on day 1 predicted the olfactory but not auditory associations that would be remembered one week later. These findings confirmed the hypothesis of a privileged brain representation for first olfactory associations.

As the scientists note, artists have long described the powerful linkage of smell and the past. Here's Marcel Proust, explaining the madeleine:

"When from a long distant past nothing subsists, after the people are dead, after the things are broken and scattered, taste and smell alone, more fragile but enduring, more unsubstantial, more persistent, more faithful, remain poised a long time, like souls, remembering, waiting, hoping, amid the ruins of all the rest; and bear unflinchingly, in the tiny and almost impalpable drop of their essence, the vast structure of recollection."

As I noted in Proust Was A Neuroscientist, these ornate subclauses contain some prophetic insights into how our brain works. In 1911, the year Proust began writing his novel, anatomists had no idea how our senses connected inside the skull - the brain was three pounds of mysterious mush. One of Proust's hypotheses, however, was that our senses of smell and taste bear a unique burden of memory. That's why he makes it clear that just looking at the seashell shaped cookie, which he'd glimpsed countless times in patisserie windows, brought back nothing; Combray remained lost. In fact, Proust even goes so far as to blame his sense of sight for obscuring his childhood memories in the first place. "Perhaps because I had so often seen such madelines without tasting them," Proust writes, "that their image had disassociated itself from those Combray days." Luckily for literature, Proust decided to put the cookie in his mouth. As he writes, it was "by taste and smell alone" that his childhood memories came flooding back.

Why is smell so sentimental? One possibility, which is supported by this recent experiment, is that the olfactory cortex has a direct neural link to the hippocampus. In contrast, all of our other senses (sight, touch and hearing) are first processed somewhere else - they go to the thalamus - and only then make their way to our memory center. This helps explain why we're so dependent on metaphors to describe taste and smell. We always describe foods by comparing them to something else, which we've tasted before. ("These madeleines taste just like my grandmother's madeleines!" Or: "These madeleines taste like the inside of a lemon poppy seed cake!") In contrast, we have a rich language of adjectives to describe what we see and hear, which allows us to define the sensory stimulus in lucid detail. As a result, we don't have to lean so heavily on simile and comparison.

It's also worth noting, of course, that the data doesn't quite support the strong version of the Proustian hypothesis. While olfactory associations enjoy a "privileged brain representation," that hippocampal link is less important than the unpleasantness of the smell, which is much better at predicting whether or not we'll remember the memory a few days later. This is the bleak truth of the brain: it clings to what we don't like.

For more, check out the work of Rachel Herz. And thanks to Jason Synder for the tip!

Read the comments on this post...