brain

An interesting story from Popular Mechanics about progress in cybernetics, titled "Mind control stories." It starts with the macaque controlling a robot arm by brain implants, and then considers the future:

For Miguel Nicolelis, a professor of neuroscience at Duke University Medical Center, the backbone of mind-machine interfaces is the ability to analyze neural activity. Sure, the system demonstrated at Pitt in May accessed information from 100 neurons at once. But Nicolelis’s lab has managed five times that amount, with data coming from up to 10 different brain structures.

For me, this is the most interesting part:

The main purpose of the walking robot experiment was to demonstrate just how precisely brain activity could be translated, but it produced another interesting result: It actually took less time for the brain signal to travel from the monkey in North Carolina to the robot in Japan than it took to go from the primate’s brain to its own muscles. At any given moment, then, the bot was receiving the command to walk before the monkey’s body did.

I've been reading Ray Kurzweil's book, and it has always seemed to me that a fundamental barrier to the development of effective neural implants is bandwidth: Human brains have evolved to use inputs and outputs at the speed of language, not the speed of electronics. So this idea of accelerating real-world responses and feedback by wiring may suggest substantial plasticity with respect to bandwidth.

I think I'll lecture on this topic in my "Biology of Mind" course this fall.

The June Scientific American (no link available) has an article on page 32 about the "therapeutic value of blogging." That's some relief, after the stories a couple of months ago about blogging being potentially deadly.

And it's no small irony, considering that the article I found on the previous two pages had great potential to give me therapeutic opportunities here.

In the article, titled, "Need for speed?" David Biello wrote up some of the human genetics results of the past 6 months, placing them as a point-counterpoint presentation of our acceleration result.

First, he cites Gregory Cochran, who does as good a job explaining our result in one sentence as I've seen:

"We found very many human genes undergoing selection" ... "We believe that this can be explained by an increase in the strength of selection as people became agriculturalists, a major ecological change, and a vast increase in the number of favorable mutations as agriculture led to increased population size."

In that form, it is hard to see how anyone could disagree. Clearly, agriculture was a major ecological shift for humans, and it imposed new selection pressures associated with diet, disease, social organization and other ecological factors. At the same time, the population grew and more people meant more mutations. That's the story; the rest is detail filled in by anthropology, genomics, and math.

Biello then cites another recent study that partially confirms our results. That study, by Lluis Quintana-Murci and colleagues, found a much smaller number of selected genes (55), but what is important is that every one of these genes has an F_ST greater than 0.65. In other words, in every one of these cases, an allele that is vanishingly rare in most of the world has reached a frequency over 80 percent in one population. As allele frequencies go, these are extreme differences -- much, much larger than the average genetic difference between populations, characterized by an F_ST around 0.1. We also found a few such alleles in our survey of selected genes, but the vast majority of genes have not generated such extreme differences in frequency -- mainly because they haven't been around long enough. In other words, the Quintana-Murci study confirms the distribution of positively selected alleles, across the range where it overlaps with other studies, including ours.

Then Biello turns to the doubters. Noah Rosenberg coauthored a study earlier this year that reported polymorphism data from a sample of populations around the world.

"We are a young species," remarks geneticist Noah Rosenberg of the University of Michigan at Ann Arbor, who participated in a comprehensive study of genetic variation that appeared in Nature in February. "Different human populations have not been separated for long enough periods of time to develop their own new alleles."

Now, I never hold quotes in the press against people, because they represent a very small portion of what they may have said to a writer, and there are many opportunities for miscommunication. Still, I have to write about this, because it's about my work! So I'll try to describe the misconceptions illustrated by the article.

I am pretty sure that Rosenberg must know that his statement in the article is false. For one thing, "developing" a new allele is simply mutation, and mutation occurs continuously. All human populations have rare alleles that have originated recently and remain distributed only across small areas. Rosenberg's surveys of gene variation have identified many such alleles.

But more important to the current question, positive selection carries an allele to high frequency very rapidly -- much more quickly than the 50,000-year or longer span of time we are talking about. An allele with a five percent fitness edge can go from zero to fixation in several hundred generations -- in humans, they can make very large frequency changes in a thousand years.

If we took the quote at face value, Rosenberg would be saying that human evolution is impossible -- and that new selected alleles like lactase persistence and sickle cell simply cannot exist. We may be a young species (although I would argue the point), but that doesn't mean that we have stopped evolving!

Two prominent geneticists quoted in the article suggest that a bottleneck may explain the pattern of human genetic variation. Here also, I have to be cautious interpreting their quotes -- because even though they may seem relevant, they are referring to their own research papers, which don't actually address the question of linkage disequilibrium and positive selection.

Marcus Feldman suggests that a series of bottlenecks are a likely explanation for the pattern of human genetic variation, in particular, the decreasing gradient of genetic diversity with increasing distance from Africa. This is the "serial founder effect" scenario that I have written about before. I criticized Feldman's and other papers on this subject this spring, referring to "the Stanford school of genetic orthodoxy." My basic point is that all of the results are assumed to support the idea of bottlenecks: no one has yet tested the hypothesis. Even simulations that show the credibility of the concept do not test the hypothesis, because they do not examine credible alternatives, either demographic or selective.

More important, bottlenecks during the dispersal from Africa 50,000 years ago cannot possibly explain linkage blocks concentrated in coding genes with a mean age of 5500 years!

Why is there such difficulty understanding natural selection? I find it quite incredible that many of the scientists who would rail against ignoring Darwin in public schools at the same time actively root out Darwin's theory from their graduate students. Still, there it is. One prominent geneticist (I won't give the name) recently asked me, "You don't really think that lactase was selected, do you?" Many really believe that natural selection has stopped and that recent human evolution reflects nothing more than the cumulative effects of bottlenecks.

What is amazing to me is that these same geneticists embrace hypotheses of population history that cannot possibly have happened. The other geneticists quoted in the article, Carlos Bustamante and his graduate student Kirk Lohmueller, wrote a paper earlier this spring arguing that deleterious mutations have reached high frequency in Europeans (moreso than Africans) because of a bottleneck during European history. The press reported this work as "Whites genetically weaker than blacks, study finds." The hypothesis in the paper is that protein-coding sites otherwise conserved in most mammals may differ among humans because of relaxed selection in a bottleneck.

Here's why they're wrong: their bottleneck is impossible. They propose that the European population was a small, isolated population of 5,700 effective individuals from 214,000 years ago up to the Last Glacial Maximum. I suppose I should take some encouragement that they believe Neandertals were European ancestors (because otherwise, where exactly would this small, isolated population of Europeans have lived). But it's still quite impossible -- it implies no gene flow between Africans and Europeans across that entire span. You see, that is the only way that genetic drift can lead to this kind of result -- large differences in frequencies between continents for hundreds of deleterious alleles. It takes a bottleneck of exceptional length, along with complete isolation.

In what has become a troubling trend, these details were hidden away in the online supplementary information of the paper. It is no surprise that most people read only the paper's conclusions, without critically evaluating the methods. But when the assumptions are hidden so that it takes an effort to look at them, you can understand that the paper does not receive the kind of scrutiny that it deserves. These are not obscure laboratory techniques; they are the basic evidence on which the conclusions were based.

Now, Bustamante knows that positive selection has been very important in recent human evolution, because he wrote an important paper on the subject in 2005. I wrote about the paper at the time -- it was one of the works that really got us thinking about acceleration in the first place. So why in the world did their more recent paper adopt such a ridiculous model of population history?

In any event, I don't think that either of these studies from earlier this year are relevant to our acceleration results. They address different aspects of genetic variation. However, acceleration may help to explain the high frequencies of some gene variants conserved in other mammals -- the results explained by Lohmueller and colleagues as relaxed selection under a bottleneck.

The acceleration of recent positive selection would predict that many otherwise conserved gene variants may be segregating in humans, because they are the targets of positive selection. These conserved sites are among those most likely to show a strong sign of recent selection, because adaptive changes on them are necessarily rare (we know they're rare, because they haven't happened very often among other species). Most such sites are still conserved in humans -- it's just not possible to change their function in adaptive ways. But the massive ecological changes of recent human history have created the opportunity for adaptive responses that are not present in other mammalian lineages. We shouldn't be surprised to see that some such changes are currently underway.

Now, that's a different interpretation of the same data, and it's a testable hypothesis. Are these conserved sites in regions that show other signs of positive selection? If they are, then acceleration explains the data. I'm looking into it now.

I've gotten a couple of e-mail questions from readers about this new book, Big Brain: The Origins and Future of Human Intelligence. The authors are Gary Lynch and Richard Granger.

Both Lynch and Granger are experts in neuroscience, with a long list of publications on memory, cortical organization, and chemical regulation of brain activity. Neither of them is an anthropologist or archaeologist.

So I suppose I shouldn't be surprised to see what appears to be complete lunacy in the book description:

Our big brains, our language ability, and our intelligence make us uniquely human. But barely 10,000 years ago--a mere blip in evolutionary time--human-like creatures called "Boskops" flourished in South Africa. They possessed extraordinary features: forebrains roughly 50% larger than ours, and estimated IQs to match--far surpassing our own. Many of these huge fossil skulls have been discovered over the last century, but most of us have never heard of this scientific marvel. Prominent neuroscientists Gary Lynch and Richard Granger compare the contents of the Boskop brain and our own brains today, and arrive at startling conclusions about our intelligence and creativity. Connecting cutting-edge theories of genetics, evolution, language, memory, learning, and intelligence, Lynch and Granger show the implications of large brains on a broad array of fields, from the current state of the art in Alzheimer's and other brain disorders, to new advances in brain-based robots that see and converse with us, and the means by which neural prosthetics-- replacement parts for the brain--are being designed and tested. The authors demystify the complexities of our brains in this fascinating and accessible book, and give us tantalizing insights into our humanity--its past, and its future.

Now, I haven't read the book, and this is not a review. I think a book that puts together the state of the art in neuroscience and tries to relate that to many aspects of human evolution would be a great book. Maybe this book has some of that stuff in it.

But it seems pretty evident from the description that there has been a major misfire. If the description of the book is accurate then they have the evolutionary biology almost entirely wrong. I assume the description is at least in the ballpark, since it is the publisher's description, and it's borne out by this Discover magazine review:

Judging from fossil remains, scientists say the Boskops were similar to modern humans but had small, childlike faces and huge melon heads that held brains about 30 percent larger than our own.

That's what fascinates psychiatrist Gary Lynch and cognitive scientist Richard Granger. "Just as we're smarter than apes, they were probably smarter than us," they speculate. More insightful and self-reflective than modern humans, with fantastic memories and a penchant for dreaming, the Boskops may have had "an internal mental life literally beyond anything we can imagine."

OK, that's a pretty surprising story: an ancient race with unique mental endowments, living in an exotic part of the world. It sounds uncannily like the Atlantis myth. What is the reality here?

First, if you do a simple Google Scholar search for "Boskop", you will discover that this has not been a going topic in human evolution for nearly fifty years. Most intellectual effort on the topic of "Boskopoids" happened between 1915 and 1930. I want to emphasize how easy it is to discover these things by a simple Google search. This is obscure knowledge, but for a good reason -- it's obsolete and has been for fifty years!

The supposed "Boskop race" was named after a South African skull -- consisting of frontal and parietal bones, with a partial occiput, one temporal and a fragment of mandible -- found on a Transvaal farm in 1913. The skull is a large one, with an estimated endocranial volume of 1800 ml. But it is hardly complete, and arguments about its overall size -- exacerbated by its thickness, which confuses estimates based on regression from external measurements -- have ranged from 1700 to 2000 ml. It is large, but well within the range of sizes found in recent males.

Robert Broom named the skull Homo capensis, emphasizing its differences from recent peoples of the region, and proposing a close relationship with European Cro-Magnons. Other remains found later were also attributed to this "type," and so the "Boskop race" became a category of paleoanthropology. Few people know that before Raymond Dart made his name by analyzing and reporting on the Taung skull, he had written in to Nature with a description of "Boskopoid" crania (Dart 1923).

But this concept of a "Boskop race" did not emerge from any clear understanding of the South African past. In fact, MSA, LSA, and recent archaeological-associated remains were lumped indiscriminately into the category. What provoked the racial category was a confusion about the relationships of recent and historical southern African remains. Anthropologists had attempted to apply primary racial categories such as "Negroid," "Bushman," "Hottentot" and "Strandloper," corresponding to extant or recent tribes or other groups. But the distinctions between these categories did not appear to extend far into the prehistoric past. So anthropologists looked for the origins of these racial types within the sample of prehistoric crania -- constructing a "Boskopoid" type for those with later "Bush" or "Strandloper" resemblances.

This category became untenable as further information about the archaeology of South Africa came to light. Ronald Singer (1958) reviewed the "Boskop race" evidence as it existed by the 1950's. He concluded that there was no reason to maintain that any "big-headed, small-faced group" had existed in prehistory, separate from the current biological variability of "Bushman, Hottentot and Negro." But that view is unsupportable -- in fact, what happened is that a small set of large crania were taken from a much larger sample of varied crania, and given the name, "Boskopoid." This selection was initially done almost without any regard for archaeological or cultural associations -- any old, large skull was a "Boskop". Later, when a more systematic inventory of archaeological associations was entered into evidence, it became clear that the "Boskop race" was entirely a figment of anthropologists' imaginations. Instead, the MSA-to-LSA population of South Africa had a varied array of features, within the last 20,000 years trending toward those present in historic southern African peoples. Singer ends his paper thusly:

It is now obvious that what was justifiable speculation (because of paucity of data) in 1923, and was apparent as speculation in 1947, is inexcusable to maintain in 1958.

That is pretty much where matters have stood ever since. "Boskopoid" is used only in this historical sense; it is has not been an active unit of analysis since the 1950's. By 1963, Brothwell could claim that Boskop itself was nothing more than a large skull of Khoisan type, leaving the concept of a "Boskop race" far behind.

Today, skeletal remains from South African LSA are generally believed to be ancestral to historic peoples in the region, including the Khoikhoi and San. The ancient people did not mysteriously disappear: they are still with us! The artistic legacy of the ancient peoples, clearly evidenced in rock art, is impressive but no more so than that of the European Upper Paleolithic or that of indigenous Australians.

And their brains were not all that big. Boskop itself is a large skull, but it is a clear standout in the sample of ancient South African crania; other males range from 1350 to 1600 ml (these are documented by Henneberg and Steyn 1993). That is around the same as Upper Paleolithic Europeans and pre-Neolithic Chinese. LSA South Africans fit in with their contemporaries around the world.

To be sure, there has been a reduction in the average brain size in South Africa during the last 10,000 years, and there have been parallel reductions in Europe and China -- pretty much everywhere we have decent samples of skeletons, it looks like brains have been shrinking. This is something I've done quite a bit of research on, and will continue to do so, because it's interesting. But it is hardly a sign that ancient humans had mysterious mental powers -- it is probably a matter of energetic efficiency (brains are expensive), developmental time (brains take a long time to mature) and diet (brains require high protein and fat consumption, less and less available to Holocene populations).

So, how did this idea of ancient Boskops make it into a book by two neuroscientists in 2008?

If not through science, then possibly from science fiction. The "Boskop race" was immortalized in popular writing by Loren Eiseley, who included an essay on Boskop Man in his collection, The Immense Journey, first published in 1958. As you can see, by this time the entire concept of a "Boskop race" had fallen into scientific disrepute. But Eiseley was undeterred: he conjured the idea that the Boskopoids were advanced in their large brains and small faces -- the apex of a trend toward paedomorphism, the retention of juvenile characteristics. In this state, they resembled what Eiseley suggested would be the "Future Man":

We can, of course, repeat the final, unanswerable question: What did this tremendous brain mean to the Boskop people? We can marvel over their curious and exotic anatomy. We can wonder at the mysterious powers hidden in the human body, so potent that once unleashed they brought this more than modern being into existence on the very threshold of the Ice Age.

We can debate for days whether that magnificent cranial endowment actually represented a superior brain. We can smile pityingly at his miserable shell heaps, point to the mute stones that were his only tools. We can do this, but in doing it we are mocking our own rude forefathers of a similar day and time. We are forgetting the high artistic sensitivity which flowered in the closing Ice Age of Europe and which, oddly, blossomed here as well, lingering on even among the dwarfed Bushmen of the Kalahari.

What we can say is that perhaps the unloosed mechanism ran too fast, that the biological clock had speeded them out of their time and place -- a time which ten thousand years later has still not arrived. This, then, was the logical end of complete foetalization: a desperate struggle to survive among a welter of more prolific and aggressive stocks.

For Eiseley, Boskop served as a kind of memento mori -- the so-called advanced race had succumbed to "more prolific and aggressive stocks." A theme of the essay is that the entire idea of "Future Man" is anti-evolutionary -- there are no ineluctible trends of progress in evolution, because such progressive populations may always be endangered by their own direction of change.

I hate to think that the theme of a 2008 book was pulled straight from a 1958 essay, but I don't know where else they would have gotten the idea. No anthropologists have written much about the so-called "Boskopoids" since 1958. There is no such thing as an "IQ estimate" for a fossil human; that's entirely nonsensical. There's no question that there have been massive cultural changes in the last 10,000 years. But the idea that our brains' functions have atrophied from some Pleistocene state has been left long behind in the dust of nineteenth-century race studies.

So I'm left wondering: Why would two neuroscientists, after going to all the trouble to write a book about the evolution of the human brain, use completely obsolete anthropological information without doing a simple Google search to see if the facts have stayed the same as in 1923?

I don't have an answer, but I'm interested in reading the book to see if it lives up to its billing.

References:

Broom R. 1918. The evidence afforded by the Boskop skull of a new species of primitive man (Homo capensis). Anthropol Pap Am Mus Nat Hist 23 (2):63-79.

Brothwell DR. 1963. Evidence of early population change in central and southern Africa: Doubts and problems. Man 63:101-104.

Dart R. 1923. Boskop remains from the south-east African coast. Nature 112:623-625.

Henneberg M, Steyn M. 1993. Trends in cranial capacity and cranial index in Subsaharan Africa during the Holocene. Am J Hum Biol 5:473-479.

Singer R. The Boskop "race" problem. Man 58:173-178.

Alan Boyle reports on the upcoming 2.0 edition of the Brain Atlas:

In the first phase, the human brain will be broken down into about 2,000 smaller structures per hemisphere. Fresh-frozen samples from up to 10 brains, selected from tissue banks around the United States, will be analyzed to produce an inventory of genes specific to each structure. Jones said the process would narrow down the focus from a total of 20,000 genes to between 50 and 500 genes per structure.

Then, researchers will build up a fine-resolution database pinpointing which high-value genes are turned on, right down to the cellular level.

The Allen Brain Atlas (no, that's not Alien Brain Atlas) currently maps gene expression in the mouse brain. I wrote about the project here last year. It's very cool -- easy to probe for genes you are interested in. But because the vast majority of genes are expressed somewhere in the brain, it is hard to get any kind of picture of whether the gene expression may be significant.

The proposal for the next version looks like it will address that problem, by looking for specific patterns of gene expression underlying different brain areas. In addition, they will add a developmental picture:

In addition to the human brain atlas, the institute plans to delve more deeply into mouse biology. A two-year, $15 million project will produce gene-expression maps for mouse brains at different stages of development, ranging from early formation to adulthood. This would help researchers see how gene expression changes over time.

It's all free for use by anybody.

Michael Balter reports on a session at the AAAS meeting about human cognitive evolution:

Richard Lewontin knows how to grab an audience's attention. Lewontin, an evolutionary biologist at Harvard University, led off a session titled "The Mind of a Toolmaker" by announcing that scientists know next to nothing about how humans got so smart. "We are missing the fossil record of human cognition," Lewontin said at the meeting. "So we make up stories."

So why did they invite him, I wonder? That's really a cranky-sounding way to start a scientific session. "All you people are just making up stories, you know next to nothing!" I mean, Richard Lewontin is certainly a well-known scientist, but he's not well known for research into the minds of early toolmakers!

On the other hand, I read what Marc Hauser apparently had to say, and I wonder...

Recent findings in his own lab and others, Hauser said, show that nonhuman animals can solve specific problems in often sophisticated ways (for example, the nectar-mapping dances of honeybees and the ability of some bird species to hide food and retrieve it much later), but they cannot apply those talents to other situations. In contrast to such "laser-beam intelligence," Hauser said, humans have evolved "floodlight intelligence" capable of adapting one solution to many new problems. Even tool use by animals--such as chimpanzees using sticks to fish for termites--is "whoppingly different" from what humans do, Hauser insisted. He hopes that the manifold human differences summarized in his "humaniqueness hypothesis" will yield clues about how our species evolved.

Hmmm.... "humaniqueness". Sounds like a perfume. If we're reduced to talking in analogies like "floodlight intelligence," maybe we really don't know anything.

References:

Balter M. 2008. How human intelligence evolved -- Is it science or 'paleofantasy'? Science 319:1028. doi:10.1126/science.319.5866.1028a

Michael Balter reports on recent research by Giacomo Rizzolatti, of "mirror neuron" fame. They taught some macaques to use pliers, and recorded what their neurons were doing:

Rizzolatti and his co-workers conclude that when learning to use a tool, the pattern of neuronal activity is somehow transferred from the hand to the tool, "as if the tool were the hand of the monkey and its tips were the monkey's fingers." As for how the same neurons could affect both the opening and the closing of the hand, the team speculates that they may be connected with other sets of neurons that more directly control these movements. The authors also point out that area F5 is rich in so-called mirror neurons, a type of nerve cell discovered earlier by Rizzolatti that fires both when a primate performs an action and when it observes another individual doing the same thing (ScienceNOW, 13 July 2007). Mirror neurons in F5, the authors suggest, may be involved in this transfer process as a monkey learns how to use a tool by watching others.

This is pretty cool, but I think its surprisingness has been overstated. A bit of reflection (har!) shows that something like mirror neurons ought to exist -- it would be far harder to build a brain capable of learning by observation if some of the same neurons weren't involved in both observing and doing. Likewise, it would be a lot more complicated to learn to use a tool if the same neurons weren't involved in planning the action using the hands compared to planning the action using a tool. So there ought to be a whole lot of neural overlap.

Now, the fact that these are in a particular region (F5) is structurally important, since this region has other functions whose interrelations aren't obvious logical necessities. And the fact that tool use is another example of a behavior that maps onto this region (at least in terms of learning) is also pretty important. It will be nice to see whether this "transfer" ability -- from hand to tool -- is a primate feature, or if instead it may be more widely distributed.

A short paper in this week's Nature finds that neurons in the human auditory cortex have an unusual capacity for perceiving small frequency differences:

Just-noticeable differences of physical parameters are often limited by the resolution of the peripheral sensory apparatus. Thus, two-point discrimination in vision is limited by the size of individual photoreceptors. Frequency selectivity is a basic property of neurons in the mammalian auditory pathway. However, just-noticeable differences of frequency are substantially smaller than the bandwidth of the peripheral sensors. Here we report that frequency tuning in single neurons recorded from human auditory cortex in response to random-chord stimuli is far narrower than that typically described in any other mammalian species (besides bats), and substantially exceeds that attributed to the human auditory periphery. Interestingly, simple spectral filter models failed to predict the neuronal responses to natural stimuli, including speech and music. Thus, natural sounds engage additional processing mechanisms beyond the exquisite frequency tuning probed by the random-chord stimuli.

The similarity with bats reminds me of a number of papers about FoxP2 -- although this is a totally different pathway. Is it about language?

This paper is totally full of jargon and extraordinarily difficult to read (and frequent readers know I wouldn't say that lightly!).

The main features are:

1. this is about the sensitivities of neurons in the auditory cortex of the brain, not anything about the ears or auditory nerves;

2. their mammalian comparisons include macaques but not apes, so it is not evident that this relates to recent human evolution (although it may);

3. the neuron responses seem to explain actual sensory acuity in humans:

These results are relevant to the apparent paradox of frequency hyperacuity demonstrated repeatedly in human psychoacoustics. Subjects with normal hearing, even untrained, successfully detect spectral differences substantially narrower than the presumed bandwidth of single auditory nerve fibres. Our results demonstrate that frequency differences smaller than 3% could be reliably detected from single-trial responses of single units in human auditory cortex. This value is comparable to the minimum detection threshold reported in untrained subjects. Thus, the responses of one of these cortical neurons could, in principle, underlie behavioural performance on a single-trial basis. Tramo et al. reported that bilateral lesions of human auditory cortex cause significant elevations in frequency discrimination thresholds, suggesting a functional role for the electrophysiological findings reported here.

4. the paper mentions that auditory fine-tuning may be related to language ability. In a press release, one of the authors suggested that the fine-tuning may be at too fine a level to be useful for language:

"This is remarkable selectivity," said Fried, who is also the co-director of UCLA's Seizure Disorder Center. "It is indeed a mystery why such resolution in humans came to be. Why did we develop this? Such selectivity is not needed for speech comprehension, but it may have a role in musical skill. The three percent frequency differences that can be detected by single neurons may explain the fact that even musically untrained people can detect such frequency differences."

I wouldn't be so quick with this interpretation. People may comprehend language despite many hearing challenges, but that doesn't mean there was no selection on hearing in association with language. Besides, speech includes a wide array of auditory information beyond words. The tonal qualities of a person's voice enable individual recognition. The fine tonal differences in a single person's speech indicate qualities such as emotional state. Plus, there are tonal languages, which may also advantage the perception of small pitch differences.

5. The last paragraph of the paper puts the auditory cortex into the context of other brain regions which have been found to have highly sensitive coding of responses in single neurons:

Previous studies in alert human subjects have shown very selective responses in single neurons from other brain areas. Notably, Quiroga et al. reported highly specific responses to individual people or landmarks from a subset of medial temporal lobe neurons, suggesting an invariant, sparse code. The high selectivity reported here may be a counterpart of the same phenomenon, resulting in a sparse coding of frequency in auditory cortex. We can only speculate why a low-level cue such as frequency is represented so explicitly and predominantly in single neurons of human auditory cortex but not in the auditory cortex of other terrestrial mammalian species.

This seems like a very interesting trend in brain research. New equipment and instrumentation allows researchers to register the outputs of single neurons, which explains why these kinds of results keep coming up recently.

If various kinds of brain processing are really organized into so-called "sparse arrays," we may need to re-evaluate the importance of gross anatomical features like brain size or the relative sizes of different brain areas. Very tiny levels of organization within brain regions may explain much of human brain evolution, with overall size -- or even the size of local regions -- being secondary.

This study also reminds us that selection on a complex structure like the brain may be accomplished along many different dimensions. Here, we see a change in the function of individual neurons, possibly enabled by local organization that functionally differentiates different neurons from each other. This is irrespective of larger structural changes to the auditory cortex, the size of the auditory cortex relative to other brain regions, the extent of lateralization of processing, or the size of the brain overall. It is also irrespective of the auditory nerve, the cochlear cells that receive sound, and the rest of the structures that influence acoustic properties of sound. Yet, every single one of those other pathways might also be targets of selection related to auditory processing; some stronger, and some weaker.

So it should be no wonder that it is hard for geneticists and neuroscientists to work these things out!

References:

Bitterman Y, Mukamel R, Malach R, Fried I, Nelken I. 2008. Ultra-fine frequency tuning revealed in single neurons of human auditory cortex. Nature 451:197-201. doi:10.1038/nature06476

I read two interesting articles today on brain performance-enhancing of one kind or another. Denise Grady of the New York Times contributes a long article about the quest for an Alzheimer's cure:

Answers are urgently needed. Alzheimer's was first recognized 100 years ago, and in all that time science has been completely unable to change the course of the disease. Desperate families spend more than $1 billion a year on drugs approved for Alzheimer's that generally have only small effects, if any, on symptoms. Patients' agitation and hallucinations often drive relatives and nursing homes to resort to additional, powerful drugs approved for other diseases like schizophrenia, drugs that can deepen the oblivion and cause severe side effects like diabetes, stroke and movement disorders.

It's a good article with lots of history about the disease and its social and economic toll. But I found this passage the most significant:

The potential market for prevention and treatment is enormous, and drug companies are eager to exploit it. If a drug could prevent Alzheimer's or just reduce the risk, as statins like Lipitor do for heart disease, half the population over 55 would probably need to take it, Dr. Thies said.

If new drugs do emerge, they will come from studies in patients who already have symptoms, Dr. Thies said. But he said the emphasis would quickly shift to treating people at risk, before symptoms set in. Many researchers doubt that even the best preventive drugs will be able to heal the brains of people who are already demented.

Treating preventively, Dr. Thies said, "will be more satisfying to patients and physicians, and there will be an economic incentive because you'll wind up treating more people."

The only thing that could slow the drive for early treatment, he said, would be serious side effects -- and Dr. Morris, at Washington University, said drugs powerful enough to treat Alzheimer's would probably have strong side effects.

It's interesting to me because of the recent genetic stuff I've been working on. But also in light of this other story in today's LA Times, by writers Karen Kaplan and Denise Gellene:

Drugs to build up that mental muscle

Academics, musicians, even poker champs use pills to sharpen their minds, legally. Labs race to develop even more.

People are already using various psychoactive drugs to get a leg up in whatever mental competitions they pursue. Some of this is no more sophisticated than late-night coffee drinking for the Ritalin generation. But some is more surprising:

"There isn't any question about it -- they made me a much better player," said Paul Phillips, 35, who credited the attention deficit drug Adderall and the narcolepsy pill Provigil with helping him earn more than $2.3 million as a poker player.

...

The growth of the brain drugs bears a striking resemblance to the post-World War I evolution of plastic surgery -- developed to rehabilitate badly disfigured soldiers but later embraced by healthy people who wanted larger breasts and fewer wrinkles.

The use of cognitive-enhancing drugs has been well documented among high school and college students. A 2005 survey of more than 10,000 college students found 4% to 7% of them tried ADHD drugs at least once to remain focused on exams or pull all-nighters. At some colleges, more than one-quarter of students surveyed said they had sampled the pills.

The article discusses the "blockbuster drug that labs are racing to develop," a memory pill. Which of course brings us full circle to Alzheimer's treatment.

You may be thinking there is something unnatural about this; maybe even something unfair -- like an athlete using steroids to enhance his performance. But with psychological factors, it is a little more evident that there is a continuum of uses, some of which are pretty clearly acceptable. For example, the performance artists who take a pill to calm their nerves before appearing on stage are literally enhancing their performance, but in a way that is arguably different from their skill as artists.

Likewise, there is a continuum among normal people -- how do we justify allowing Adderall for the student who has trouble taking an eight-hour exam, but denying it to the student who had trouble sleeping before the exam?

Progress on these kinds of drugs will only come with understanding the continuum of psychological and cognitive variation among living people -- along with the causes of that variation, both developmental and genetic. We might like some chemical to increase memory performance. But the brain is a complicated place with countless interactions of different structural and regulatory processes. Maybe some people already have the chemicals that enhance memory, and other people don't, or don't express them in the right places in the right amounts. If so, then Alzheimer's treatment may focus on the metabolic processes of non-Alzheimer's brains, for example.

Plus, as we've learned recently with respect to traumatic stress, it's not always good to remember things well, so there is no reason to assume that the human population has been adapting toward longer or better memory. In general, it's not obvious exactly what memory characteristics have tended to increase fitness recently or during earlier phases of human evolution. Aside from the energy and life history constraints of large brains, we don't know what evolutionary trade-offs exist with respect to memory or other aspects of cognitive function.

Athletes take performance-enhancing drugs for a relatively slight advantage. Pharmaceutical firms are pursuing brain drugs on the expectation that millions of people will take a daily pill for years on end, in order to stave off Alzheimer's. Unshackling the mind power of a large proportion of the older population will no doubt have a tremendous impact on the societies of the future.

Pretty exciting stuff, if only we could figure it out.

There's a house in my neighborhood that puts on a giant show every Halloween, with graves, ghosts, and horror-show music. We call it the "Halloween house", and it has everything you would need for a haunted house except jello brains. A few years ago, my daughter Sophie was thrilled by the Halloween house, talking about it all the way up to October 30.

Then, the excitement turned to fear. All around the neighborhood Halloween night, she was clearly in denial. She managed to put the house out of her mind up to the end of the sidewalk leading up to the house, where the combination of the imminent creepiness and the slasher music had her quaking in her shoes.

We didn't get treats at the Halloween house that year, or the next.

This is the season for thinking of fear -- I was briefly quoted in our student newspaper about the evolution of fear. But Mo of Neurophilosophy does a much better job of describing the related neural circuitry.

They key region is the amygdala, and memory is intimately involved. There is some new progress on the genetics of the mechanisms:

Recently, however, Gleb Shumyatsky and his colleagues at Rutgers University in New Jersey discovered several genes that are highly expressed in the amygdala, and which appear to be involved in this process. One of these encodes a protein called stathmin (also known as oncoprotein 18), which is now known to be involved in mediating the formation of memories of both conditioned and unconditioned fear. There is a high level of expression of the stathmin gene, and a corresponding high concentration of stathmin protein, in the amygdala, but not in the adjacent hippocampus.

Mutant mice lacking the stathmin gene were unable to learn new fears or to act instinctively in a fearful situation, i.e. they had weaker memories of fearful experiences. The stathmin knockout mice also showed less anxiety when presented with new mazes to explore or with potentially dangerous situations. Upon further examination, it was observed that mice lacking the stathmin gene had a less dynamic microtubule network than wild type (normal) mice.

This year, we got treats from the Halloween house, even my 2-year-old. I think the younger ones were mainly influenced by the bravery of the eldest. Also, they cut out the spooky slasher-movie music. No Michael Myers hiding in the bushes.

I really like that quote, by computer security expert Bruce Schneier. The context, though, is sort of silly:

He told delegates at the 2007 RSA Conference that there is a gap between the reality of security and the emotional feel of security due to the way our brains have evolved. This leads to people making bad choices.

"As a species we got really good at estimating risk in an East African village 100,000 years ago. But in 2007 London? Modern times are harder."

Uhh...so it seems to me if you really believed that, you would advocate computers that properly trigger our anachronistic system of risk detection. Like maybe they could give a leopard-like screech when we choose a password of less than six letters?

Or, uhh...maybe you could just make them secure in the first place?

Still, it's interesting to see this idea about human evolution spreading around out there through the world. The "anachronistic brain":

"The brain is still in beta mode, it's got all sorts of patches and workarounds. It's not perfectly created, it's clearly evolved up."

In other words, cruft.

Schneier emphasizes our inaccurate assessments of small risks, proposing that we did much better in our "natural" habitat. I'm not so sure about that -- remember, I'm running a slow-moving series on risk. There's no particular reason to think that our assessments of ancient risks should have been accurate, since accurate risk assessment is not the same as fitness-maximizing risk assessment.

Translate that into the modern environment: Schneier seems to be claiming that the main feature of the modern risk environment is very slight, impersonal, uncontrollable risk margins. Sounds like the flip side of profit-taking opportunities. Maybe we'll evolve safer computers yet.

An Amanda Schaffer article, "In Diabetes, a Complex of Causes" in the Science Times covers recent research on Type 2 diabetes. The interesting part of the research is the extent that insulin resistance and related hormonal signaling have been linked to processes ranging from inflammation, bone metabolism, and the brain:

In previous work, Dr. Karsenty had shown that leptin, a hormone produced by fat, is an important regulator of bone metabolism. In this work, he tested the idea that the conversation was a two-way street. "We hypothesized that if fat regulates bone, bone in essence must regulate fat," he said.

Working with mice, he found that a previously known substance called osteocalcin, which is produced by bone, acted by signaling fat cells as well as the pancreas. The net effect is to improve how mice secrete and handle insulin, the hormone that helps the body move glucose from the bloodstream into cells of the muscle and liver, where it can be used for energy or stored for future use. Insulin is also important in regulating lipids.

The common theme seems to be this: Once, doctors focused on easy-to-measure biomarkers, like blood glucose level. But these are in turn affected by many different physiological processes -- far from the pancreas --- many in feedback relations regulated by multiple signaling molecules.

The brain in particular exerts a powerful drain on blood glucose. So you might expect something like this:

"If the brain is getting the message that you have adequate amounts of these hormones and nutrients, it will constrain glucose production by the liver and keep blood glucose relatively low," said Dr. Michael W. Schwartz, a professor at the University of Washington. But if the brain senses inadequate amounts, he continued, it will "activate responses that cause the liver to make more glucose, and new evidence suggests that this contributes to diabetes and impaired glucose metabolism."

There's a lot more, although the article doesn't touch on the recent genomic scans for diabetes-related genes.

I often lecture to my 100-level classes on human adaptations to altitude and the effects of hypoxia. Our picture of these adaptations and other physiological changes associated with high altitude has been changing in recent years. One reason is a better assessment of the variability among high-altitude populations in their response to hypoxia.

The other reason is better technology. The "Mind Matters" feature of the Scientific American blog has a feature this week on the neuroscience of altitude sickness. It details some of the effects of hypoxia on the brain, including details from recent studies involving MRI scans of elite climbers:

This acute high-altitude disease has long been known to cause brain damage. But one of the sobering things about the Fayed study is that none of the Everest climbers experienced high altitude cerebral edema, and the only acute case of mountain sickness was a mild one suffered by the expedition's amateur climber. Yet even all the professional mountaineers showed lasting brain damage -- presumably suffered on previous ascents to the high mountains, because their MRI scans were abnormal before the Mt. Everest ascent and unchanged after.

The essay is by R. Douglas Fields, describing work by Nicholas Fayed and colleagues. The results are true not only for Everest but for lower-altitude summits as well. The first discussed is Aconcagua:

The body is remarkably resilient--does the brain recover from these mountaineering wounds? To answer this important question, the researchers re-examined the same climbers three years after the expedition, with no other high-altitude climbing intervening. In all cases, the brain damage was still evident on the second brain scan.

Still, Aconcagua is one of the world's highest mountains -- in the top 100. Mont Blanc, in the Alps, is less extreme. With a summit at 4810 meters, it is climbed each year by thousands of mountaineers who probably do not expect injury to their "second favorite organ," to use Woody Allen's nomenclature for the brain. Yet the researchers found that of seven climbers reaching the summit of Mount Blanc, two returned with enlarged VR spaces.

Of course, if you've seen any of the various Everest documentaries, you will remember the cognitive impairment that results from low oxygen. Climbers often can't think straight, and particularly inexperienced climbers really need someone at a lower altitude to help supervise their summit attempts. But the sobering thing about these MRI results is that the altitude of Mont Blanc is substantially lower than the Everest base camp at 5500 meters.

Welcome, everyone, to the twenty-second edition of the neuroscience carnival, Encephalon. Never in my life have I received so many e-mails with the subject line, "Submission". Whoa! I checked the spam filter to make sure they weren't going into the wrong bin.

Meanwhile life intervened, and we're starting a day late here, but you'll see we're not a dollar short -- with 11 contributions.

Ome sweet ome

Bohemian Scientist, who has to have the coolest banner ever, writes an ode to the -ome:

it's not news that scientists aren't all linguists. but that ain't no excuse for the nominal slop that pervades biological appelation. perhaps the most notorious of cases, and the subject of today's exposé, begins in the 1920s: flappers were a dime a dozen, histologists were still arguing over the neuron doctrine, and a forty-something german botanist was coining the term genome. with it, he unwittingly hacked open a pandora's box of lingual lament, unleashing the phoneme-turned-meme -ome to a world poised to beat it to death. the inevitable ome-philia is now as annoyingly crazy as its shakespearean counterpart; one can only wish it were as self-destructive.

The suffix has invaded neuroscience, with the "connectome" and Bohemian Scientist may not be ready for the change! Of course, this is a topic I hit last year -- my complaint being that people were doing genomics without bothering to learn genetics. I suspect that will be true in neuroscience as well -- why learn about the brain when you're really studying the connectome?

Sounds like a drinking game

The Neurocritic writes in with two posts on the neural correlates of attention. The first, "Bottoms Up" reviews a paper on top-down versus bottom-up attention. The second, "Tops Down" describes some experiments intended to localize aspects of the conscious control of perception:

Unique opportunities to record intracranially in awake behaving humans occur clinically in the neurosurgical arena, to monitor for seizures in patients with intractable epilepsy (Dubeau & McLachlan, 2000). In a series of such experiments in the mid-90's, Halgren and colleagues recorded local field potentials from over two thousand cortical and subcortical sites...

Read on to see what they found.

Making faces

Pure Pedantry's Jake Young also enters two articles. In "Do autistic people have a deficit in reading faces?", he reviews research that shows that an original conclusion was not as simple as it appeared:

In the Thatcher illusion, two picture of Margaret Thatcher's face are inverted. One has (in the inverted form) the mouth and eyes turned right-side-up. The faces are then rotated such that now one of the faces is correct and the other is right-side-up with the mouth and eyes now inverted....

This discrepancy -- the feeling of wrongness associated with the altered right-side-up face -- is due to a preference in the human visual system for correctly oriented faces. Originally, it was believed that people with autism lacked this discrepancy -- the difference in the wrong feeling between the inverted Thatcher face and the correctly oriented with upside down mouth and eyes Thatcher face -- suggesting a general deficit in face processing.

This one is worth looking at for the links to the weird Margaret Thatcher faces alone! The second post, "Monkey Economics" has a connection to the Freakonomics guys, capuchin monkeys, and money. What more could you ask for?

A dramatic turn

Neurophilosophy's MC goes deeper into the world of Dostoyevsky with a post on Saint Vitus's Dance:

In The Idiot, Myshkin's epilepsy is first mentioned in chapter one. In the online edition of the book, which I quoted in the post about Dostoyevsky's epilepsy, his condition is described as "some strange nervous malady - a type of epilepsy, with convulsive spasms." But in McDuff's translation, the same passage reads slightly differently; Myshkin is said to suffer from "some strange nervous illness akin to epilepsy or St. Vitus's Dance, with tremors and convulsions." This aroused my curiosity - I'd never before heard of Saint Vitus's Dance, so I decided to investigate further.

The intersection of history and neuroscience also infuses the post, "Old Brains, New Ideas". This is a really good presentation of the recent reevaluation of the brains of Paul Broca's patients -- the ones that led him to identify what we now call Broca's area:

Dronkers and her group re-examined the brains using high resolution magnetic resonance imaging (MRI). Although two neuroimaging studies have recently been performed on Leborgne's brain, Lelong's brain has remained unexamined, since the nineteenth century, in the Paris museum.

This re-examination revealed that, in both Leborgne and Lelong, the most extensive damage is not in the part of the frontal lobe most often designated as Broca's, but rather in the region just anterior to it - thus, the area considered by Broca to be crucial for speech atriculation is not the same as the region that is today called Broca's area. Further, in both Leborgne's and Lelong's brains, the damage extended far deeper than the lateral surface of the frontal lobe than Broca's reports suggested, and it is probable that these deeper lesions contributed to the speech deficits that the patients presented with.

Some mainstream micro

On the subject of historical rediscoveries, journalist Michael Balter writes in with his recent article in Science titled, "Brain evolution studies go micro."

If you didn't get a chance to read this article when it came out, take advantage of Michael's free link to it, on his list of articles.

There's no welt like umwelt

Chris Chatham's Developing Intelligence takes a stroll in the sensory system of a bat:

In his famous essay, Thomas Nagel suggested that science's reductionist methods can never provide a complete understanding of the "subjective qualities" of consciousness. To illustrate this problem, he wrote that there was "no reason to suppose that" we would ever be able to comprehend what it's like to be a bat - because we can't truly understand the subjective experience of, for example, echolocation.

Ironically, scientific advances in "sensory substitution" technology have demonstrated that it's possible to simulate (or stimulate) one modality (sight, hearing, touch) with sensory data from another.

Will "sensory substitution" lead to new technologies to supplement the senses? Augment human consciousness? Fight the Penguin?

The timekeeper inside

From Bora's Blog Around the Clock, we have a review of "clock" genes. These genes underlie circadian rhythms, and as a recent paper shows, their action is modulated by network effects in the suprachiasmic area (SCN) of the brain:

And what they found, over and over, is that particular genetic knock-outs eliminate rhythms in individual cells (both SCN and peripheral), and in peripheral tissues, yet intact SCN tissue remains rhythmic and whole animal even more so. A peripheral clock is a collection of cells, a pacemaker is a network of cells.

Bora's background post on the basics of biological clocks is good background to his summary of the cutting-edge research.

Cephalized is centralized

Our next host, Madam Fathom, investigates the early evolution of the central nervous system in vertebrates compared to their hypothetical ancestor, Urbilateria:

The striking similarities between these two animals, separated by hundreds of millions of years of evolution, implies a common evolutionary origin from an equally complex ancestral pattern. In other words, Urbilateria must have had these same sets of genes, in the same spatial orientation, patterning its nervous system, which must have likewise been centralized. Of course, this is still a matter of probability, but it seems highly unlikely that such a complex arrangement of genes could have been recruited independently to specify evolutionarily unrelated cell populations.

Read on to discover the identity of this animal, and what it tells us about the genetic patterns underlying the development of the central nervous system.

The next edition, Encephalon 23, will be hosted by Madam Fathom on May 21. You may send submissions directly there, or to encephalon.host [at] gmail.com.

At last, someone may have the courage to try to harness the brainpower of the superintelligent fearless mice.

And that someone is...IBM!

US researchers have simulated half a virtual mouse brain on a supercomputer.

The scientists ran a "cortical simulator" that was as big and as complex as half of a mouse brain on the BlueGene L supercomputer.

In other smaller simulations the researchers say they have seen characteristics of thought patterns observed in real mouse brains.

Now the team is tuning the simulation to make it run faster and to make it more like a real mouse brain.

I'm thinking two things: First, this is a neuron-level interaction simulation; so it will be interesting to see what kinds of phenomena can be modeled accurately at that level, and what kinds require subcellular or genetic controls that aren't modeled here.

Second, I'm wondering how the heck the BBC manages to write stories where every sentence is its own paragraph!

I mean, every single one!

But seriously, the question of gene-level interactions (with differential expression in different neuron types, and different brain regions) versus purely network-scale interactions will be an interesting emerging question from work like this, particularly since we have the mouse brain gene expression atlas.

This is too weird:

Thus when dogs were attracted to something, including a benign, approachable cat, their tails wagged right, and when they were fearful, their tails went left, Dr. Vallortigara said. It suggests that the muscles in the right side of the tail reflect positive emotions while the muscles in the left side express negative ones.

That's from a NY Times article by Sandra Blakeslee. The whole article's about this dog tail-wagging emotional asymmetry.

And then there is all this:

Honeybees learn better when using their right antenna, she said. Male chameleons show more aggression, reflected as changes in body color, when they look at another chameleon with their left eye. A toad is more likely to jump away when a predator is introduced to its left visual field (right brain/fear). The same toad prefers to flick its tongue to the right side when lashing out at a cricket (left brain/ nourishment).

Chicks prefer to use their left eye to search for food and right eye to watch for predators overhead, Dr. Rogers said. But when chicks are raised in the dark, they do not develop normal brain asymmetry. In trying to eat and watch for hawks overhead, such nonlateralized chicks become confused and vulnerable to attack.

Now that's one messed-up experiment. Chicks raised in the dark, suddenly put out in the open where hawks are circling overhead.

Hmmm:

And left-handed chimps are more fearful of novel stimuli than right-handers. Their dominant right brains may make them more cautious.

The article ends with a bunch of adaptive-sounding explanations for asymmetry and lateralization of "approach and withdrawal" traits, but nothing very convincing. Personally, I would guess the mechanism is essentially like gene duplication: you get two copies of something, and one of them may mutate to take on new functions. Lateralization should be favored as a pathway above functionally redundant brain structures.

But then, there seems to be incredible plasticity to much of brain development, including lateralization in humans. Maybe lateralization in humans has high plasticity because enlarged human brain sizes are comparatively recent -- there hasn't been a lot of time for the evolution of functional lateralization in the new volume of the neocortex. As it becomes clearer what is new and what is old in the human brain, there will be the chance to test hypotheses about the origins of lateralized functions.

Another of the papers in PNAS online this week is this one:

Human relational memory requires time and sleep

Jeffrey M. Ellenbogen et al.

Relational memory, the flexible ability to generalize across existing stores of information, is a fundamental property of human cognition. Little is known, however, about how and when this inferential knowledge emerges. Here, we test the hypothesis that human relational memory develops during offline time periods. Fifty-six participants initially learned five "premise pairs" (A>B, B>C, C>D, D>E, and E>F). Unknown to subjects, the pairs contained an embedded hierarchy (A>B>C>D>E>F). Following an offline delay of either 20 min, 12 hr (wake or sleep), or 24 hr, knowledge of the hierarchy was tested by examining inferential judgments for novel "inference pairs" (B>D, C>E, and B>E). Despite all groups achieving near-identical premise pair retention after the offline delay (all groups, >85%; the building blocks of the hierarchy), a striking dissociation was evident in the ability to make relational inference judgments: the 20-min group showed no evidence of inferential ability (52%), whereas the 12- and 24-hr groups displayed highly significant relational memory developments (inference ability of both groups, >75%; P < 0.001). Moreover, if the 12-hr period contained sleep, an additional boost to relational memory was seen for the most distant inferential judgment (the B>E pair; sleep = 93%, wake = 69%, P = 0.03). Interestingly, despite this increase in performance, the sleep benefit was not associated with an increase in subjective confidence for these judgments. Together, these findings demonstrate that human relational memory develops during offline time delays. Furthermore, sleep appears to preferentially facilitate this process by enhancing hierarchical memory binding, thereby allowing superior performance for the more distant inferential judgments, a benefit that may operate below the level of conscious awareness.

This suggests two things to me:

1. It actually should work to think about a problem in the evening, go to bed, and then think about it again in the morning. This actually seems to work fairly well for me, so I find it entirely plausible.

2. The standard 15-minute scientific talk is just the right length for nobody to remember anything at the end.

This passage from the discussion is a mini-review:

It is interesting to note the similarity between this finding and recent evidence implicating sleep in the enhancement of memory associations (23), the development of flexible, creative information processing (24, 25), and the relational building of component motor-sequence memories (15, 17, 18). Together, these data provide a new and emerging role for sleep in facilitating associative integration of information, a form of memory binding or extracting experience generalities. A potential candidate structure orchestrating these associative effects might be the hippocampus. Numerous studies have emphasized the dependence of transitive inference on the hippocampal integrity (1). Considering that the hippocampus has consistently been implicated in offline memory reprocessing, manifest in neuronal "replay" following learning (e.g., see ref. 26), a speculative hypothesis is that similar neural reactivation during offline periods of wake and (especially) sleep facilitates relational mapping between learned items. Therefore, such offline hippocampal reprocessing may underlie not only the strengthening of individual item memory, but the binding, and hence subsequent flexible use and expression, of acquired declarative memories (Ellenbogen et al. 2007:7727).

They also cite some research that indicates that people can learn relational hierarchies without being consciously aware of them, which seems relevant to social cognition in non-human primates as well as humans.

References:

Ellenbogen JM, Hu PT, Payne JD, Titone D, Walker MP. 2007. Human relational memory requires time and sleep. Proc Nat Acad Sci USA 104:7723-7728. doi:10.1073/pnas.0700094104

This article in last week's Science seems interesting:

Top-Down Versus Bottom-Up Control of Attention in the Prefrontal and Posterior Parietal Cortices

Timothy J. Buschman and Earl K. Miller

Attention can be focused volitionally by "top-down" signals derived from task demands and automatically by "bottom-up" signals from salient stimuli. The frontal and parietal cortices are involved, but their neural activity has not been directly compared. Therefore, we recorded from them simultaneously in monkeys. Prefrontal neurons reflected the target location first during top-down attention, whereas parietal neurons signaled it earlier during bottom-up attention. Synchrony between frontal and parietal areas was stronger in lower frequencies during top-down attention and in higher frequencies during bottom-up attention. This result indicates that top-down and bottom-up signals arise from the frontal and sensory cortex, respectively, and different modes of attention may emphasize synchrony at different frequencies.

At the end, they speculate that this difference in frequency has to do with the greater transmissibility of low frequency signals across different areas.

Lower-frequency bands are more robust to spike timing delays and thus may be better suited for longer-range coupling between multiple, distant areas (28-30). The increase in low-frequency synchrony during search could reflect a "broadcast" of top-down signals on a larger anatomical scale.

That's a simple information theoretic argument; the idea being that a low-rate signal is more resistant to degradation by noise across brain areas.

References:

Buschman TJ, Miller EK. 2007. Top-down versus bottom-up control of attention in the prefrontal and posterior parietal cortices. Science 315:1860-1862. doi:10.1126/science.1138071

I just wrote about the alteration of a behavior pattern (decision-making) resulting from injury to the prefrontal cortex. That is the kind of functional specificity that might be expected as a result of "modularization" of mental functions. In that case, injuries to different people in the same place have the same kind of effect on behavior. Arguably, some part of the ventromedial prefrontal cortex functions as a module involved in moral decision-making (and as I noted, decision-making applied to gambling and other kinds of risks).

In a different study this week, a research team created knock-in mice, expressing the human photopigment allowing trichromatic vision in humans and other primates. They found that, even though mice belong to a lineage that hasn't had trichromatic vision for more than 100 million years, the mice immediately started perceiving the new color.

Here's an account from New Scientist, by Roxanne Khamsi:

The study demonstrates that the mouse brain is "primed" for expanded colour vision, the researchers say. It suggests that a simple mutation giving rise to the L receptor protein in our primate ancestors immediately expanded their visual perception.

"It has been unclear whether the simple addition of a photopigment is sufficient to yield a new dimension of colour vision, or whether you might need, in addition, some changes in the nervous system," says Gerald Jacobs, a vision researcher at the University of California, Santa Barbara, US, who took part in the study.

This is very interesting because it means that simple mutational changes in sensory systems are readily incorporated into sensory and cognitive processes by the brain. The paper suggests that the occurrence of novel sensory receptors might lead to selection for more and more efficient mechanisms for discriminating information, based on an initial, imperfect effect. That is basically the explanation for the evolution of all sensory systems, and is a powerful one.

The addition of new sensory receptors may be even more relevant for smell than for sight, since smell depends on hundreds of different olfactory receptor proteins, which originated by duplications and are eliminated by deactivations in different lineages of mammals. In retrospect, the idea that a novel sensory receptor might have immediate effects is sort of obvious, considering that humans are polymorphic for many olfactory receptors and some taste receptors. People with red-green colorblindness don't have catastrophic failure of their visual perception; instead, the perception system develops normally in the context of the lack of information from the missing receptor. Likewise, the senses of smell and taste bootstrap themselves based on the information present throughout development.

It's not remarkable that the brain should be plastic to new inputs; we would have noticed much sooner if it weren't!

References:

Jacobs GH, Williams GA, Cahill H, Nathans J. 2007. Emergence of novel color vision in mice engineered to express a human cone photopigment. Science 315:1723-1725. doi:10.1126/science.1138838