In the 1950s and ’60s, several villages in the Oceanic country of Papua New Guinea began to see an odd disease. Villagers of the Fore people in the Eastern Highlands - predominantly women and children - would show an array of frightening symptoms that rapidly worsened over about six months: muscle tremors, uncontrollable laughter, slurring of speech and finally an inability to move and swallow. In the 1960’s, European scientists began to study people with the disease, called kuru for the Fore word for “shiver,” and made two astonishing discoveries. First, that kuru represented a new kind of infectious disease that caused the brain and nervous system to degenerate. Second, that kuru probably resulted from people eating their dead relatives.

Yeah, that’s not a typo. Before the Fore people of Papua New Guinea were known for kuru, they were known for “mortuary feasts,” where villagers would mark the death of a family member by consuming him or her. And not just a nibble here or there - according to a 1979 book by anthropologist Shirley Lindenbaum, “meat, viscera, and brain were all eaten.” That’s a good way to spread a disease caused by prions - the mechanism for kuru eventually discovered by Daniel Carleton Gajdusek in research that won him the 1976 Nobel Prize in Physiology or Medicine. Now, kuru continues to fascinate the scientific community, as a new medical paper presents how the savage disease caused rapid natural selection in Papua New Guinea, selecting for a gene variant that may offer clues to how to treat prion diseases with no known cure.

Prions are also the culprit behind bovine spongiform encephalopathy, better known as Mad Cow Disease, which is thought to have broken out in Britain due to cannibalistic feeding practices in cattle. In short, prion diseases are caused by misshaped proteins that are a bad influence on native prion proteins present in all species, causing them to change shape, clump together, and eventually kill the cell. So when a prion disease enters a person’s nervous system - by, say, eating a person with a prion disease - it tends to wreak havoc in the brain, producing the odd symptoms of kuru or BSE.

At the height of kuru, 1 out of 50 people in some Fore villages succumbed to the untreatable, fatal disease. Women and children tended to die more often from kuru, likely because they usually were given the brains to eat while the men got the good, meaty parts. But what about those who participated in the mortuary feasts, but never contracted the disease? Was there something genetically different about them that made them resistant? Sounds like a case for…evolution!

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Until indoor smoking bans started popping up in cities across the country in recent years, smoke-filled bars were a fixture of American culture, smoking and drinking entwined like the peanut butter and jelly of vices. If you were a casual scientist of the street, you might have hypothesized that there was something meaningful behind the common sight of the barfly with a drink in one hand and a cigarette in the other. And laboratory research has mostly supported that anecdotal evidence, with study after study showing that alcohol does in fact promote smoking behavior, while larger surveys have found alcoholics more likely to be smokers and vice versa. But where do the effects of a beer and a cigarette meet in the brain, such that ordering up one raises a person’s desire to partake of the other?

That’s been one of the questions studied in the Clinical Addictions Research Laboratory at the University of Chicago Medical Center, where director Andrea King has examined the phenomenon of alcohol-induced smoking. The studies put the spotlight on an interesting population of smokers - not the pack-a-day regulars, but those who smoke “socially,” a few cigarettes on nights out on the town with friends. That’s a demographic that hasn’t received as much study as addicted smokers, King said, in part due to psychiatric guidelines that classified people as either smokers or non-smokers with no space for people in the gray areas.

“Older studies wouldn’t even ask how frequently subjects smoked; if they smoke, they must be addicted, daily smokers,” said King, an associate professor of psychiatry and behavioral neuroscience. “But we see this percent that seems to be increasing in subsequent surveys…about 20-30 percent would be non-daily smokers. Some of these people may continue and become vulnerable to being a chronic habitual user, or this may be a new subclass of smokers.”

King was drawn to social, alcohol-induced smoking behavior when she was attempting to recruit heavy drinkers who were not smokers for a control group, a task she found exceptionally difficult. With rates of smoking among alcoholics as high as 75 percent, the non-smoking drinker was a rare breed, so King decided to flip it around to study what causes the two behaviors to frequently co-exist.

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A sleeping zebra finch (courtesy of Margoliash lab)

One of the repeated themes of the Darwin/Chicago 2009 meeting two weeks ago was the history of the anti-evolution movement, a resistance that has actually changed form, even *cough* evolved, quite a bit since The Origin of the Species. At the opening night event in Rockefeller Chapel, science historian Ronald Numbers talked about differences between the anti-Darwinists led by William Jennings Bryan in the 1920’s (immortalized in the Scopes Monkey Trial and Inherit the Wind) and today’s intelligent design supporters and creationists. Surprisingly, Bryan and his followers were considerably less extreme than today’s anti-evolutionists, as Numbers explained that most who railed against Darwinism in the early 20th century were fine with the evolution of animals over billions of years, they merely could not abide that humans also evolved.

The evolution vs. creation debate has obviously become a lot more complicated since then, but Bryan’s primary objection has lingered - the core of most people’s opposition to evolution is the idea that humans must be somehow separate and different from the rest of the natural world. One “proof” of this uniqueness is the complexity of human language, a form of communication that, to the casual observer, appears in an entirely different league from the songs, gestures, or simple noises that animals use to share information. The assumption that the more complex forms of human language are unique is even held by some in the field of linguistics and psychology, including the legendary Noam Chomsky, who argued as much in a 2002 Science paper with cognitive psychologist (and Darwin/Chicago speaker) Marc Hauser.

That assumption is a handicap to the study of language, argue University of Chicago’s Daniel Margoliash and Howard Nusbaum in a recent issue of the journal Trends in Cognitive Science. The idea that human language is biologically unique, and thus the kind of “hopeful monster” geneticist Richard Goldschmidt coined to describe the sudden appearance of a new feature in evolutionary history, walls off language from the world of biology. Perceiving human language in its proper evolutionary context, and thus exposing it to the tools of comparative biology, will allow scientists to fully understand how language works and where it originated, Margoliash and Nusbaum conclude.

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I spent part of last week on vacation from science in Las Vegas, where I thankfully avoided financial ruin due to some fortunate combination of genes, math awareness and a wife that has no interest in gambling. Sure, I dabbled a bit in games of chance, but as soon as I got a little bit ahead on the blackjack tables I ran for my life, knowing that the probability would even out hard in the long run. For those concerned about the financial well-being of Sin City, they still managed to turn a profit on us, thanks to the low-return temptations of fine dining and French circus acts set to Beatles megamixes. But most of our time was spent on the free entertainment of people-watching and stuff-watching, observing row after row of people almost hypnotically at work on loud, noisy slot machines amid fake New York, Paris and Venice scenery.

It doesn’t take a PhD in neurobiology to conclude that slot machines are designed to lure people into a money-draining repetition, just as it doesn’t take expertise in the casino business to realize slots are absurdly profitable - there’s a reason why they outnumber table games 100-to-1. But I wanted to go back to the scientific literature to confirm a faint glimmer of information I retained from graduate school, specifically that slot machines are masterful manipulators of our brain’s natural reward system. Every feature - the incessant noise, the flashing lights, the position of the rolls and the sound of the coins hitting the dish - is designed to hijack the parts of our brain designed for the pursuit of food and sex and turn it into a river of quarters. Or so I remember.

Fortunately, there is a robust amount of research into why slot machines are so addictive, despite paying out only about 75% of what people put in. They are, some scientists have concluded, the most addictive of all the ways humans have designed to gamble, because pathological gambling appears faster in slots players and more money is spent on the machines than other forms of gambling. In Spain, where gambling is legal and slot machines can be found in most bars, more than 20.3 billion dollars was spent on slots in 2008 - 44% of the total money spent by Spaniards on gambling last year.

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5:00 p.m. - Biomedicine and Bracketology

Here’s the final report from today’s session, join us again tomorrow for a full Halloween day of evolutionary science and philosophy! Also, continue to follow PZ Myers of Pharyngula and Skip Evans of Wisconsin Citizens for Science for their reports on the conference.

Both talks in the final session of the day focused on how the incredible advances in gathering genetic information over the last decade have done much to shake up the worlds of genetics and evolutionary biology. As we’ve written about previously, the 1959 conference helped solidify what’s known as the modern synthesis of evolution that incorporated the then-new information about DNA, genes and molecular mechanisms of inheritance, an arrangement that forever married the two fields. Well, could the participants in that conference have predicted that 50 years later we would have a reasonably complete genome for humans, not to mention 43 other vertebrate species? And did they know how much trouble it would cause?

Eric Lander, who was one of the leaders of the Human Genome Project, said he felt slightly out of place at a conference about Darwin, but the modern synthesis marriage sometimes makes strange bedfellows! Regardless, Lander’s talk was a great primer on how the dogma of genetics has been forever altered by what we learned from the HGP and the genomes of other animals: that we have far fewer genes than we thought (~20,000 vs. previous estimates of 100,000), that much of what is handed down between generations is “non-coding” DNA that doesn’t make proteins, that those “non-coding” sections may create important regulatory elements that help organisms develop. Lander, who described himself as a biomedical scientist, said much of what has been found since the explosion of genetic data has been bad news for medical geneticists - many disease-associated alleles have been found, but most have very marginal effects on the probability of a person developing that disease. But Lander said it was a glass half-full/half-empty situation:

“Those people who want to do personal genomics - take your DNA and tell you your risk of diabetes - they’re in trouble. This is not going to be the best way to do that,” Lander said. “But if I want to understand what diabetes is about…I start to get clues to the pathways that matter to diabetes.”

The final talk of the day covered how genetics has caused a similar reshuffling in the field of phylogeny - the science of organizing life into “trees” that show the evolution and relationships of species. Philip Ward, from UC-Davis, talked about the durability of the “Tree of Life” simile, which Darwin readily used in Origin of Species - the only figure in the book is an early phylogenic tree. Modern phylogeny produces beautifully complex trees that look like 10,000-team basketball tournaments run in reverse, with the winner being life’s common ancestor. But as biologists have turned to genetics to build these trees, they’ve found that they lead to completely different trees than the ones built from morphology, the physical characteristics of organisms.

One reason for this is a tricky effect called convergence - two species that are not closely related and live continents apart could form a resemblance because they evolved in similar environments. Ward studies a type of ant that is found in both Asia and America, and morphology would suggest that they are closely related species despite being so far apart geographically. However, genetic data showed the ants were more distantly related than previously could have been estimated from their looks, suggesting they evolved to look similar due to their similar environments, without a recent common ancestor.

But the Tree of Life remains a strong structural model, Ward said. So strong, in fact, that it has been adopted by creationists, who describe an “orchard of life” of animals that evolved after Noah’s flood. As with most mentions of creation “science” at the meeting, Ward’s slides about these theories drew mostly giggles from an audience decidedly on the side of Darwin, even as genetics reveals a world more complex than he ever could have imagined.

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Studies of human disease often work from the patient backwards - doctors and scientists take the common symptoms of a particular disorder and use them as clues to figure out what first went awry to spur the disease. For neurological diseases like Parkinson’s or amytrophic lateral sclerosis (aka Lou Gehrig’s Disease), symptoms and brain images have pointed the research at particular parts of the brain, which are then studied in animal models and on the genetic or cellular level. But disease research can also work from the other direction, where a particular cellular process is identified as a potential culprit in the disorder before a patient with that defect is even found.

That’s the case with a paper published this month by a team of University of Chicago researchers studying the cellular mechanisms that underlie diabetes. There are many types of diabetes mellitus, but all can be traced back to the hormone insulin - the body’s signal that cells should soak up sugar from the blood. Most cases of juvenile, or Type 1, diabetes result from the immune system erroneously attacking and killing the Beta-cells of the pancreas, which release insulin. Type 2 diabetes, which often develops in adulthood, results from a reduced sensitivity to insulin and/or a decreased release of the hormone.

But diabetes can also have a genetic origin, in some rare cases, when one of the genes involved in the secretion of insulin is disrupted. Previously on the blog, we’ve talked about the story of Lilly Jaffe, whose diabetes was found to be caused by a rare genetic mutation in a protein called a potassium channel, critical for the release of insulin. The mutated potassium channel seen in Lilly’s case interferes with the trigger of insulin release, causing lower amounts of the hormone to circulate through her blood. Thus, Lilly was treated by daily injections of insulin, until doctors at the University of Chicago detected the mutation and prescribed her a drug that directly targeted the potassium channel.

Now researchers at the University of Chicago have found another ion channel that must function properly for the right amount of insulin to be released. Only problem: there’s no patient.

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And so Neuroscience 2009 comes to an end, and it’s time to put away my badge, rest my weary feet and note-taking hand and think about biology below the neck again. Here’s the final installment of our live coverage, but come back tomorrow for a roundup of the conference with highlights, loose observations and links to other people’s thoughts on the conference. Thanks for reading!

2:30 PM - The Final Talk

The schedule may say that Neuroscience 2009 runs through the end of the day today, but judging by how many suitcase-toting scientists were jumping in airport cabs this afternoon, a small portion of the 30,000+ attendance makes it to the very end. Indeed, even the main stage ends its conference early, shutting down after a talk by Mt. Sinai School of Medicine’s Eric Nestler, an expert in the field of molecular psychiatry.

Nestler’s research focuses on the gritty details of how drugs of abuse change the expression of a person’s genes - yes, it was another addiction talk, and the former addiction researcher that I am, it was great to see the topic getting so much attention this year. In the addiction press conference I attended yesterday, Nestler hinted at a bombshell idea - frequent users of addictive drugs such as cocaine, heroin or alcohol may change the mechanics of their genes so permanently, the modifications could be passed on to their children. This “inheritable addiction” has already been observed in lab rats, Nestler said, mirroring similar results seen with the offspring of obese rats (which I talked about on Monday).

But that data must be too fresh for mass consumption, despite Nestler telling a roomful of reporters about it the day before. His talk today focused on the steps leading up to that discovery, carefully examining how repeated cocaine increases or decreases the activity of hundreds of genes in the reward pathway of the brain. Those long-lasting changes, which can cause cells of the reward pathway to actually grow and change shape, help explain why addiction is such a difficult condition to treat - it may require a complete re-re-structuring of the brain.

Much of the addiction research I’ve talked about this week has taken place in animals, but before Nestler’s talk, I came across a rare experiment that looks at the behavioral effects of a commonly-used drug in humans. It might seem strange that we know a ton about the specific genes that are up or down-regulated by cocaine, but not so much about its effects upon humans, but that’s due to procedural reasons - it’s quite hard to get approval for a study that gives illegal drugs to humans.

Michael Ballard, from the University of Chicago laboratory of Harriet DeWit, was trying to fill in at least one of those gaps in the research by testing the effects of THC (the active ingredient in marijuana) to presumably eager volunteers. Ballard then tested the subjects’ ability to judge facial expressions and determine the emotional content of pictures and personality trait words while they were under the influence of the drug. Interestingly, higher doses of THC caused the subjects to misjudge the facial expressions they were shown, suggesting an effect of the drug on social perception. The other tests were normal during the drug effect, but when brought back to the laboratory a week later, the subjects showed a decreased ability to remember neutral and negative personality traits, possibly indicating that their memories of the drug effect were biased toward happier stimuli. Ballard hopes to continue that research into other drug types - he’s currently testing amphetamine - to give the field of addiction research much-needed, laboratory-controlled human data to make sense of the flood of animal experiments.

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6:45 PM - The Opposite of a History Lesson

Eric Kandel is 80 years old, was present at the first Society for Neuroscience meeting in 1969, is 9 years removed from winning the Nobel Prize for physiology and medicine. He’s also so well known at the Neuroscience meeting, he can go by one name, “like Bono,” said SfN president Tom Carew in his introduction to tonight’s Presidental Lecture. So you might have expected Kandel’s talk to be a history lesson, a retelling of how he uncovered the cellular chain of events that underlie learning and memory in sea slugs, fruit flies, mice and, by extension, you and me.

But Kandel, looking like The Sopranos’ Uncle Junior and speaking with Woody Allen’s Brooklyn accent, had very little interest in looking back. After 75 minutes of him excitedly flashing through graphs and figures explaining recent findings in his laboratory at Columbia University, he could only narrow his talk down to four conclusions. My thesis adviser, who was sitting next to me, leaning over and whispered in amazement, “these aren’t conclusions at all, he’s still forging ahead.”

That relentless drive in someone so late in his career was infectious. Kandel said the goal of his talk was to explain how a person remembers his first love for the rest of his life, as if that was a simple quest, but his lecture portrayed science as it should be: a never-ending story, with each answer giving birth to several more questions. While some researchers settle on a single technique and pass the torch to younger researchers when the limits of that technique are reached, Kandel proved that he has stayed on the cutting edge of science, bringing fresh talent into his lab to apply new tools to his endless questions about how neurons encode memory.

As a result, almost a decade after his Nobel victory, Kandel was excitedly telling 10,000 of his colleagues about a new cellular signal, called CRB-3 in mice, which he humbly described as “a new class of functional proteins” and “an entirely new model of synaptic plasticity.” The work was backed up with the latest in genetic, cellular biology and imaging evidence, testimony to both Kandel’s ability to keep up with the fast-moving world of science as well as the sprawling world of neuroscience itself.

“One of the wonderful things that has happened in my forty years in the society, is that neuroscience, which really was quite fragmented when I entered the field…has become a unified organism,” Kandel said.

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6:30 PM - Taking Drugs Like Driving Without Brakes

The day ended with another emissary from the NIH, as Nora Volkow, director of the National Institute on Drug Abuse, gave the week’s third Presidential Lecture. I’ve heard Volkow speak a couple times now - I was actually at NIDA when she was named director in 2002 - and I’ve always found her work to be some of the most convincing data available about addictive drugs change the way the human brain works. The operative word there is human, since most studies of drug addiction (including my own work) has been performed in animals, and there are several nagging questions about the human relevance of research in animals on complex behaviors like addiction.

The directorship appears to be keeping Volkow busy with administrative duties rather than scientific work, as much of the talk was unchanged from when I saw it seven years ago. But the story is still a good one, using imaging of a particular neurotransmitter system in the brain, dopamine, to search for differences in the brains of people who habitually use drugs and people who don’t. Dopamine is increased in response to drugs of abuse, and without getting too technical, Volkow found that one type of dopamine receptor, called D2, is severely reduced in people who repeatedly use drugs such as cocaine, heroin and alcohol. Simultaneously, another region called the prefrontal cortex (PFC) shows reduced activity in drug addicts. The role of the PFC is to control people’s impulsivity - Volkow described it as the part of the brain that told her not to have a glass of wine before her talk. So repeated exposure to a drug such as cocaine can actually remove a person’s natural control of impulses, leading to more drug use and binge drug-taking behavior.

“You basically disrupt any ability to control that drive,” Volkow said, “So the person is really without brakes, and is unable to stop taking the drug.”

but the more recent data indicated an interesting flip as relatives of alcoholics, who don’t drink themselves, also show lower D2 receptors and PFC activity. So it creates a chicken and egg situation - do addicts lower their D2 receptors, or do lower D2 receptors predispose a person to become addicted to drugs. Regardless, coming closer to understanding this relationship means that improved therapies for addiction may not be far off.

And with that, I’m off to the dopamine party, made up of dopamine researchers raising their own dopamine via drinking, listening to music and social interaction. See you tomorrow.

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4:00 PM - What Makes a Man, Mr. Lebowski?

Sex differences appeared to be the unintentional theme of the day, as the press conference I sat in on focused on biology and behavior specific to males. This is an interesting scientific double-reverse - as Arthur Arnold had said earlier in his special lecture, most of neuroscience (and science in general) has experimented on males, which has created occasional problems in applying those results to females. For at least the past decade, that imbalance has been remedied, with most animal studies including both male and female subjects. But that doesn’t meant that aren’t interesting questions remaining about the male brain, and this conference brought together Arnold and four researchers working in that sub-field.

Despite the message of Arnold’s talk earlier (”sex difference is more than just hormones”), the research largely focused on how testosterone - the hormone produced by the male testes - affects behavior. Two of the studies (both from the University of Wisconsin) utilized an interesting animal model, California mice, whose males display two curious behaviors. One, presented by Matthew Fuxjager, is “the winner effect,” a phenomenon where mice that have won fights with other mice are more likely to win subsequent fights. Fuxjager found that the brains of California mice are full of triggers for testosterone, including areas normally associated with reward. “Winning can in fact change the brain,” Fuxjager concluded, a relevant message for an NFL Sunday.

Erin Gleason also uses California mice in her research, but instead of focusing on their fighting habits, she looks at their parenting. The mice are one of the few rodent species where the father and mother share in the care of their pups, and Gleason looked at the role testosterone plays in this behavior. Surprisingly, removing testosterone (by, well, castration) actually decreased the mouse fathers’ parenting skills - the same hormone so intricately involved in making a mouse a good fighter also made them a good Dad, it seems. Moreover, when Gleason looked at the offspring of those castrated dads later in life, they themselves were bad fathers despite no experimenter manipulation of their hormones. Lax parenting was inherited, and hormonal effects rippled down a generation.

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As described on Monday and hinted at all week, this weekend marks the start of Neuroscience 2009, the annual mega-conference of more than 30,000 neuroscientists. After years of staging the meeting in areas with distractingly nice climates such as New Orleans, Orlando and San Diego, this year should be all business with the rainy chill of Chicago keeping people indoors. But there’s still a lot of fun to be had, with big-time speakers, immersive poster sessions, the never-ending hunt for the best vendor knick-knack giveaway and the night-time socials. Because of Neuroscience’s massive size, there are a million different ways to navigate a path through the science, but here’s a quick extremely long guide to what I’m looking forward to experiencing. Remember to tune in to ScienceLife all weekend (and through Wednesday) for coverage.

Saturday: Magicians Were the First Neuroscientists

Each year one of the most interesting lectures falls under the sober heading of “Dialogues Between Neuroscience and Society,” which basically means “we invited someone from outside of neuroscience to talk about neuroscience.” At previous meetings I’ve attended, that meant hearing public figures such as the Dalai Lama and Frank Gehry offering their own perspective on the brain, the mind and thinking - necessary reminders that the microscopic neurons those 30,000 scientists are concentrated on actually add up to some pretty amazing things in practice. 

This year’s Dialogues speakers are neuroscientists of a different sort: magicians Apollo Robbins and Eric Mead. Even though I saw a local version of this talk earlier this year with Robbins and neuroscientist Susana Martinez-Conde (which I wrote about it for the Tribune), I’m excited to see it again, because it really is a neat demonstration of how magicians have used the brain’s limitations to produce convincing illusions. Robbins, whose act is centered on his considerable abilities as a pickpocket, is a master of using diversion to direct a person’s attention one direction while he slips off their watch from another angle. As Robbins and Martinez-Conde explained back in January, this deceptively simple trick actually says a lot about how the brain shifts attention from stimulus to stimulus, and how a normal brain is “tricked” may help us learn about the neurobiological process that underlie an attentional disorder like ADHD. You can watch a video of a similar symposium organized by Martinez-Conde back in 2007 called “The Magic of Consciousness” - which includes Teller of Penn & Teller in a rare speaking role.

Also Saturday: We’re only two weeks away from the University of Chicago’s big Darwin conference, but I still will probably take in at least part of the symposium on Evolution of Brain and Behavior. Harvard’s Elizabeth Spelke caps off the day with a lecture on how the brain processes math - thankfully, it’s scheduled early in the conference, before my own brain will surely grow too tired to handle such a heavy topic.

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The classic slogan for Lay’s potato chips is “Betcha’ can’t eat just one!,” and anyone who’s ever sat down with a new bag of chips and systematically worked their way down to the bottom of the bag in an almost hypnotic state knows the truth of that message. Portion size has been shown in many studies to be a contributor to overeating, as scientists find that people tend to eat the food that’s placed in front of them rather than stopping when their hunger is satisfied. Some might say this behavior is culturally programmed by millions of mothers telling children to “clean their plates” - a good strategy for broccoli, but a rather unhealthy one when faced with a heaping mound of french fries.

But there may also be a biological reason driving people to eat whatever amount of food is placed in front of them, to the detriment of their own personal health. Today in the Journal of Neuroscience, University of Chicago neurobiologists Hayley Foo and Peggy Mason publish experiments that indicate rats get into a zone while eating or drinking something they like that actually reduces their sensitivity to pain. While eating a chocolate chip or having sugar water or regular water infused into their mouths, rats are slower to move their feet away from a hot light-bulb than when they are not eating or drinking. The implication is that rats are so focused on finishing the food in front of them, they are less susceptible to distractions…such as, for instance, a hot foot.

“It’s a strong, strong effect, but it’s not about hunger or appetite,” Mason said. “If you have all this food in front of you that’s easily available to reach out and get, you’re not going to stop eating, for basically almost any reason.”

In the wild, where food is scarce, a resistance to distraction while eating is a good skill to have. If a wild rat is eating a hard-earned nut, it would rather ignore that mild pain in its foot rather than flee the scene and risk losing the nut to another hungry animal. But for humans in modern society, where the next meal is only as far as the nearest supermarket or McDonald’s, an unshakable focus on finishing the food in front of you and drowning out distractions (like a little voice inside your head reminding you how many calories you’re consuming in that Big Mac), is decidedly unhealthy.

“We’ve gotten a lot more overweight in last 100 to 150 years,” Mason said. “We’re not more hungry; the fact of the matter is that we eat more because food is readily available and we are biologically destined to eat what’s readily available.”

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Laughter is almost universal. It’s an expression that is seen across all human cultures, babies begin to laugh within the first few months of life, and animals such as apes and even rats exhibit forms of laughter. The ubiquity of laughter suggests that it’s a behavior that dates far back in human cultural history and evolution – and that you might be able to trace laughter back to some of the most basic parts of our brains.

The neurobiological roots of laughter will be the focus of a lecture this Saturday by University of Chicago professor of neurology and psychology Steven Small built from the latest discoveries in brain imaging research. But Small’s lecture won’t be happening at the big Neuroscience meeting at McCormick Place, but as a special part of the Chicago Humanities Festival. Small, appearing from 10:00 – 11:00 Saturday, Oct. 17 at the Max Palevsky Cinema in Ida Noyes Hall, 1212 E. 59th St., said he will give a talk for non-scientists on the strange but primal act of laughing, including where it appears to be localized in the brain and what can happen to make this simple act go awry.

Small, whose own research focuses on the neurobiology of language, said he has not studied laughter himself, but found the behavior to be an intriguing example of the brain at work. Gathering material for his talk led him to discover popular 1920’s novelty records of people laughing, medical case studies of uncontrollable laughter caused by neurological diseases and tales of a contagious laughing epidemic in Tanzania that lasted as long as one week in some children.

For his lecture, “Humor Humours, Laughter and the Brain,” Small said he will focus on laughter itself and its relation to emotional expression, which is not always related to what people find funny – a distinction that actually makes neurobiological sense.

“Laughter as a response to humor is what we think of, but that’s not what laughter is. It’s a reflex.” Small said. “It’s a motor sequence and a sound sequence, and it can be produced by a mechanism that doesn’t even have to be controlled by the cerebral cortex. You don’t need to have a cognitive stimulus: I could tickle you, and you would laugh. It doesn’t have to have humor involved at all. Of course, its association with emotion, social exchange, and humor is what makes laughter in humans different from laughter in other animals.”
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Because of limitations in funding and expertise, most laboratories choose to become skilled in one particular technique, be it behavior, molecular biology or electrophysiology – the practice of recording electrical activity in neurons. But as neuroscientists get closer to resolving some of the most complex mysteries of the brain, some researchers find themselves increasingly reaching the limits of those chosen methods. A behavioral researcher might wonder what cellular processes mediate the performance of an animal on a learning task, while a scientist studying neurons in isolation can only speculate about what those microscopic observations mean in an intact organism.

“Really the major problem in neuroscience right now is defining what is the underlying cause,” said Daniel McGehee, associate professor of anesthesia and critical care (and, full disclosure, my former thesis advisor).

The solution to that problem is collaboration, said McGehee and Xiaoxi Zhuang, associate professor of neurobiology, and a recent publication by the two researchers is a vivid example. Published late last month in the Journal of Neuroscience, their study of how an intracellular signal expressed in only one region of the brain mediates certain types of learning could only have been done by combining the strengths of their two laboratories.

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(photo courtesy of Nature)

Bruce Lahn knew that his 2005 papers on the recent evolution of brain genes might stir up some controversy. In the journal Science, the University of Chicago professor of human genetics and his colleagues studied two genes involved in regulation of brain size during development. Intriguingly, they found variants of these genes that are favored by natural selection and are more prevalent in some geographic groups than others. Despite caveats about the complex, multi-dimensional nature of genetic differences, Lahn expected that people on the fringe might twist his research to justify racist beliefs. But he was  surprised at the degree of controversy, particularly the negative reaction from other scientists who distorted his conclusions to make straw-man arguments and even questioned the worth of doing such research in the first place.

That experience, Lahn says now, made him wiser about the way that human genetics research is interpreted by the public and even his scientific peers. But rather than shy away from the type of research that provoked such hubbub, Lahn decided that scientists needed a new moral framework to deal with rapidly growing information about how genes differ between individuals and groups. In an opinion piece published in the journal Nature today, Lahn and co-author Lanny Ebenstein argue that scientists and society at large must embrace the idea of genetic diversity, rather than persist in the more palatable assumption, increasingly disproven by science, that there are no meaningful genetic differences between geographic and ethnic human groups.

“I think the danger really is in the moral attitudes of the people themselves,” Lahn said when we discussed his essay earlier this week. “Instead of trying to suppress the science we should try to build a moral consensus that is constructive to the overall well-being of the species. I think that’s what’s important.”

“The truth about human diversity cannot be changed, but attitudes can change,” he continued. “I think it’s better to change attitudes than to hide factual truths.”

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