Links for Keyword: Genes & Behavior

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By Tina Hesman Saey WASHINGTON — Separation anxiety in some children may be due to extra doses of a particular gene. The gene, GTF2I, is located on human chromosome 7. People missing part of the chromosome that contains GTF2I have a condition called Williams syndrome and are generally extra social. On the other hand, people who have extra copies of that part of chromosome 7 may have social and other types of anxiety: About 26 percent of children with an extra copy the region containing GTF2I have been diagnosed by a doctor as having separation anxiety, human geneticist Lucy Osborne of the University of Toronto said November 15 at a press conference at the Society for Neuroscience’s annual meeting. Osborne and colleagues genetically engineered mice to have a duplicate copy or two of GTF2I, or to be missing one copy of the gene, then tested the effect of the gene dosage on separation anxiety with a squeak test. Week-old baby mice separated from their mothers send out ultrasonic distress calls. “It’s a ‘come get me’ signal,” Osborne said. Baby mice with a normal two copies of GTF2I squeaked an average of 192 times over four minutes when removed briefly from their nests. Mice with three or four copies squeaked nearly twice as much, indicating greater anxiety at being separated from their mothers. Mice missing one copy of the gene were a little bit less vocal. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 16051 - Posted: 11.19.2011

By Laura Sanders Human brains all work pretty much the same and use roughly the same genes in the same way to build and maintain the infrastructure that makes people who they are, two new studies show. And by charting the brain’s genetic activity from before birth to old age, the studies reveal that the brain continually remodels itself in predictable ways throughout life. In addition to uncovering details of how the brain grows and ages, the results may help scientists better understand what goes awry in brain disorders such as schizophrenia and autism. “The complexity is mind-numbing,” says neuroscientist Stephen Ginsberg of the Nathan Kline Institute and New York University Langone Medical Center, who wasn’t involved in the studies. “It puts the brain in rarefied air.” In the studies, published in the Oct. 27 Nature, researchers focused not on DNA — virtually every cell’s raw genetic material is identical — but on when, where and for how long each gene is turned on over the course of a person’s life. To do this, the researchers measured levels of mRNA, a molecule whose appearance marks one of the first steps in executing the orders contained in a gene, in postmortem samples of donated brains that ranged in age from weeks after conception to old age. These different patterns of mRNA levels distinguish the brain from a heart, for instance, and a human from a mouse, too, says Nenad Šestan of Yale University School of Medicine and coauthor of one of the studies. “Essentially, we carry the same genes as mice,” he says. “However, in us, these genes are up to something quite different.” © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15961 - Posted: 10.29.2011

Despite vast differences in the genetic code across individuals and ethnicities, the human brain shows a "consistent molecular architecture," say researchers supported by the National Institutes of Health. The finding is from a pair of studies that have created databases revealing when and where genes turn on and off in multiple brain regions through development. "Our study shows how 650,000 common genetic variations that make each of us a unique person may influence the ebb and flow of 24,000 genes in the most distinctly human part of our brain as we grow and age," explained Joel Kleinman, M.D., Ph.D., of the National Institute of Mental Health (NIMH) Clinical Brain Disorders Branch. Kleinman and NIMH grantee Nenad Sestan, M.D., Ph.D. of Yale University, New Haven, Conn., led the sister studies in the Oct. 27, 2011 issue of the journal Nature. genetic difference vs. transcriptional distance colored by race comparison. Our brains are all made of the same stuff. Despite individual and ethnic genetic diversity, our prefrontal cortex shows a consistent molecular architecture. For example, overall differences in the genetic code (“genetic distance”) between African -Americans (AA) and caucasians (cauc) showed no effect on their overall difference in expressed transcripts (“transcriptional distance”). The vertical span of color-coded areas is about the same, indicating that our brains all share the same tissue at a molecular level, despite distinct DNA differences on the horizontal axis. Each dot represents a comparison between two individuals. The AA::AA comparisons (blue) generally show more genetic diversity than cauc::cauc comparisons (yellow), because caucasians are descended from a relatively small subset of ancestors who migrated from Africa, while African Americans are descended from a more diverse gene pool among the much larger population that remained in Africa. AA::cauc comparisons (green) differed most across their genomes as a whole, but this had no effect on their transcriptomes as a whole. Source: Joel Kleinman, M.D., Ph.D., NIMH Clinical Brain Disorders Branch

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15960 - Posted: 10.29.2011

By Tina Hesman Saey A genetic variant that makes small tweaks in an important brain protein may cause aging to hit some people’s brains harder than others. Pilots’ performance on a flight simulator test generally declines slightly with age. But a new study shows that pilots with a particular version of a gene called BDNF have a faster drop than others. Researchers also observed a decline in the size of an important learning and memory center in the brains of those with the variant, Ahmad Salehi of the Department of Veterans Affairs Palo Alto Health Care System and Stanford University, and colleagues report online October 25 in Translational Psychiatry. About 38 percent of pilots in the new study carried the variant in either one or both of their copies of the BDNF gene. Over the course of two years the flight simulator scores of all the pilots in the study declined a little with age. But scores of pilots carrying the variant dropped about three times faster than scores of pilots who have the normal version of the gene. The drop in scores was not so dramatic that pilots should be removed from the cockpit, says Salehi. “It certainly did not disable them at all,” he says. But the score drop did reflect a slightly faster decline in factors like reaction time, navigation skills, plane positioning and performance in emergency situations. For some of the pilots, the researchers measured the size of the hippocampus, a structure in the brain that is important for learning and memory. After age 65, men who had the alternate version of the gene also lost more hippocampus volume than men with the normal version of the gene, the researchers found. The size of the hippocampus did not correlate with scores on flight simulator tests, probably because flying a plane requires much more of the brain than just the hippocampus, Salehi says. © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 15953 - Posted: 10.27.2011

Jonathan Weitzman As an identical twin, I have always been fascinated by what determines who we are. Nature's clones are never truly identical, so what explains the differences between my brother and myself? How much of our identity is inherited; how much acquired by interacting with the environment? The field of epigenetics, standing at the interface between our environment and our genes, is beginning to offer answers. Epigenetics explores how genetically identical entities, whether cells or whole organisms, display different characteristics, and how these are inherited. The past century witnessed amazing advances in our understanding of genetics, but secrets remain hidden within the genome. Epigenetics research is now blossoming, offering a potential panacea for these post-genome blues. Two timely books open up this emergent field: Epigenetics by Richard Francis and The Epigenetics Revolution by Nessa Carey offer very different takes. Francis's thoughtful and succinct book focuses on the narrative and the excitement of discovery, rather than on the nitty-gritty details at the molecular level. His personal tour includes anecdotes from his travels around the world and allusions to popular culture. Carey's book is more DNA-centric, focusing on epigenetic mechanisms and the chemistry of chromatin, which defines how DNA is packaged around proteins in the nucleus. Her book combines an easy style with a textbook's thoroughness. © 2011 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15857 - Posted: 09.29.2011

By Lauren Ware In a clear Plexiglas laboratory cage, a mouse sleeps. A thin fiber optic cable projects upward from the top of its head and out through the cage’s lid. The cable lights with a pulse of blue light. The mouse continues to sleep; the light continues to pulse. After a few more pulses, the mouse wakes up. It rubs its face, stretches its legs and runs over to its food cup and begins to eat voraciously, as though it were starving. It keeps eating as the blue light pulses. The optical fiber that carries the blue light goes directly into the mouse’s brain. It targets a specific group of brain cells that have been modified to react to light. The experiment uses a technique called optogenetics, developed seven years ago, which can selectively activate or silence groups of nerve cells, or neurons, in real time. And it allows scientists to interact with the brain and begin to map how it works with a degree of detail that was previously unimaginable. That’s what Scott Sternson has done with the apparently starving mouse at Janelia Farm in Ashburn, Va., an interdisciplinary biomedical research center that is part of the Howard Hughes Medical Institute. In fact, this mouse was well fed and should not have been hungry. Sternson’s research group targeted a type of cell called the agouti-related peptide (AGRP) neuron. AGRP cells live in the hypothalamus and have been linked to feeding behavior in other studies. The scientists used a virus to insert the DNA of a light-sensitive protein from bacteria, channelrhodopsin-2, into the AGRP neurons. Some of the AGRP neurons take up the DNA and begin to produce the protein and send it to the cell membrane. When the blue light is flashed into the mouse’s brain via the optical fiber, the protein causes the neurons to move ions across the cell membrane, effectively stimulating them to fire an electrical signal, the action potential, which neurons use to communicate with each other. Sternson found that the more AGRP neurons are stimulated, the more the mouse eats. And as soon as the light stops, so does the feeding. Miller-McCune © 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 15792 - Posted: 09.13.2011

McMaster University researchers have discovered that a key gene may explain why some people are energetic and others find it hard to get moving. The team was working with mice, some of which had two genes removed. The genes control the AMP-activated protein kinase (or AMPK), an enzyme that is released during exercise. While mice like to run, the mice without the genes were not as active as mice with the genes. "While the normal mice could run for miles, those without the genes in their muscle could only run the same distance as down the hall and back," Gregory Steinberg, associate professor of medicine in the Michael G. DeGroote School of Medicine and Canada Research Chair in Metabolism and Obesity, said in a release Monday. "The mice looked identical to their brothers or sisters, but within seconds we knew which ones had the genes and which one didn't." The researchers found the mice without the AMPK genes had lower levels of mitochondria — sometimes described as cellular power plants — and their muscles were less able to take up glucose while they exercised. By removing the genes, the researchers found that AMPK is the key regulator of the mitochondria, said Steinberg. The research is in the current issue of the Proceedings of the National Academy of Sciences. © CBC 2011

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15768 - Posted: 09.06.2011

A new atlas of gene expression in the mouse brain provides insight into how genes work in the outer part of the brain called the cerebral cortex. In humans, the cerebral cortex is the largest part of the brain, and the region responsible for memory, sensory perception and language. Mice and people share 90 percent of their genes so the atlas, which is based on the study of normal mice, lays a foundation for future studies of mouse models for human diseases and, eventually, the development of treatments. Researchers from the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, and from Oxford University in the United Kingdom, published a description of the new atlas in the Aug. 25, 2011, journal Neuron. The study describes the activity of more than 11,000 genes in the six layers of brain cells that make up the cerebral cortex. To map gene activity in all six layers of the mouse cerebral cortex, the research team first micro-dissected the brains of eight adult mice, separating the layers of the cortex. They then purified processed RNAs, including messenger RNA, from each cortical layer. The international collaborators have made the new atlas freely available at http://genserv.anat.ox.ac.uk/layers.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 15717 - Posted: 08.25.2011

by Sarah C.P. Williams Lab mice usually take only an occasional jaunt on their exercise wheels. But mice missing a gene called IL-15Rα run for hours each night, a new study reveals. And the gene doesn't just make a difference to mice—it might also be linked to the ability of long-distance athletes to outperform the rest of us. Previous studies had suggested that IL-15Rα is important for muscle strength. In experiments on cells grown in a Petri dish, the gene seemed to control the accumulation of proteins necessary for muscle contraction. But IL-15Rα had never been studied in a living animal. In the new research, physiologist Tejvir Khurana of the University of Pennsylvania and his colleagues genetically engineered mice to lack the IL-15Rα gene. The changes were dramatic. Each night, according to sensors on the wheels in the mice's cages, the modified mice ran six times farther than normal mice. But these behavioral quirks weren't quite enough to convince Khurana of the effect on muscles. Lack of the IL-15Rα gene could just be making the mice jittery or giving them extra energy. So the researchers dissected muscles from the longer-running mice. The muscles sported increased numbers of energy-generating mitochondria and more muscle fibers, indicating that they tired less easily. And when the researchers stimulated them with electricity, the muscles continued to contract for longer than normal, taking longer to use up their energy stores, the team reports today in The Journal of Clinical Investigation. © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15572 - Posted: 07.19.2011

Erika Check Hayden Two years ago, 13-year-old Alexis Beery developed a cough and a breathing problem so severe that her parents placed a baby monitor in her room just to make sure she would survive the night. Alexis would often cough so hard and so long that she would throw up, and had to take daily injections of adrenaline just to keep breathing. Yet doctors weren't sure what was wrong. In a paper published today in Science Translational Medicine1, researchers led by Richard Gibbs, head of the Baylor College of Medicine Human Genome Sequencing Center in Houston, Texas, describe how they sequenced the genomes of Alexis and her twin brother, Noah, to diagnose the cause of her cough — a discovery that led to a treatment. Today, Alexis is playing soccer and running, and her breathing problem has gone, says Alexis's mother, Retta. "We honestly didn't know if Alexis was going to make it through this," Retta Beery says. "Sequencing has brought her life back." At age 5, the Beery twins had already been diagnosed with a genetic disorder called dopa-responsive dystonia, which causes abnormal movements, and had been taking a medication that was apparently successfully treating the condition. When Alexis developed a worsening cough and breathing problem, the twins' neurologists did not think it was related to her dystonia. © 2011 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 15433 - Posted: 06.16.2011

By Steve Connor, Science Editor Women have a stronger genetic predisposition to help other people compared with men, according to a study that has found a significant link between genes and the tendency to be "nice". The research, based on an analysis of nearly 1,000 pairs of identical and non-identical twins, found that about half of "prosocial" traits – the willingness to help others – identified in women could be linked with genes rather than environmental upbringing, whereas the figure was just 20 per cent in men. Scientists believe the findings lend further support to the idea that prosocial behaviour has a strong heritable component with some people displaying an innate tendency from childhood. One conclusion from the study, published in the journal Biology Letters, is that some women, and rather fewer men, find it easier than the rest of the population to be generous and helpful towards others, given the right sort of upbringing. "There is a very big debate at the moment about whether humans are altruistic or not," said Gary Lewis, a psychologist at the University of Edinburgh who carried out the research. "There are some people who argue that we have evolved to be altruistic independently of external interventions, and others who argue that we are rather selfish and need a rather conducive external environment for us to be nice to others. ©independent.co.uk

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 14980 - Posted: 02.10.2011

A tiny, translucent water flea that can reproduce without sex and lives in ponds and lakes has more genes than any other creature, said scientists who have sequenced the crustacean's genome. Daphnia pulex, named after the nymph in Greek mythology who transforms into a tree in order to escape the lovestruck Apollo, has 31,000 genes compared to humans who have about 23,000, said the research in the journal Science. Often studied by scientists who want to learn about the effects of pollution and environmental changes on water creatures, the almost-microscopic freshwater Daphnia is the first crustacean to have its genome sequenced. But just because this creature -- viewed as the canary in the gold mine of the world's waters -- has more genes doesn't necessarily mean they are all unique, explained project leader John Colbourne. "Daphnia's high gene number is largely because its genes are multiplying, by creating copies at a higher rate than other species," said Colbourne, genomics director at the Center for Genomics and Bioinformatics. Daphnia has a large number of never-before seen genes, as well as a big chunk of the same genes found in humans, the most of any insects or crustacean so far known to scientists. "More than one-third of Daphnia's genes are undocumented in any other organism -- in other words, they are completely new to science," said Don Gilbert, coauthor and Department of Biology scientist at IU Bloomington. © 2011 Discovery Communications, LLC.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 14963 - Posted: 02.07.2011

By Neil Bowdler Science reporter, BBC News Researchers in the United States say they have uncovered tentative evidence of a genetic component to friendship. Using data from two independent studies, they found carriers of one gene associated with alcoholism tended to stick together. However, people with another gene linked with metabolism and openness, stayed apart. Details are published in the journal Proceedings of the National Academy of Sciences. The researchers looked at six genetic markers in two long-running US studies, the National Longitudinal Study of Adolescent Health and the Framingham Heart Study, which contain both genetic data and information on friends. With one gene, called DRD2, which has been associated with alcoholism, they found clusters of friends with the very same marker. Another gene called CYP2A6, which has a suspected role in the metabolism of foreign bodies including nicotine, appeared more divisive. People with this gene seemed to steer clear of those who also carry the gene. Why, the researchers don't know, but they speculate it could form part of a defensive ploy. They say similar patterns have been observed among couples, with individuals avoiding prospective partners who are susceptible to the same diseases. BBC © MMXI

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 14900 - Posted: 01.21.2011

A person's friends tend to share certain genes in common with each other — but not always with the individual, a new study suggests. "People’s friends may not only have similar traits, but actually resemble each other on a genotypic level," said the study led by James Fowler, a geneticist at the University of California at San Diego. The findings were published Friday in the Proceedings of the National Academy of Sciences. Researchers noticed two distinct patterns within social networks when it came to the genes DRD2, which has been linked to alcoholism, and CYP2AP, which is linked with the character trait of openness. In the case of DRD2, people with the marker tend to make friends with those who also have that marker. People without it tend to make friends with other DRD2-negative individuals. In the case of CYP2A6, the person who has the gene tends to be the hub of a social network made up of people who don't have it and instead share the opposite genotype. Four other genes examined by the researchers did not show such patterns among groups of friends. The analysis found that this gene clustering within social networks was apparent even when the researchers took into account the fact that people are more likely to make friends with people who live near them. The findings suggest that studies linking certain traits to genes may be biased in ways that were not previously anticipated. © CBC 2011

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 0: ; Chapter 13: Memory, Learning, and Development
Link ID: 14885 - Posted: 01.18.2011

Jennifer Couzin-Frankel In the fall of 2008, Stephen Kingsmore, a longtime gene hunter, was approached by two biotech entrepreneurs. One of them, Craig Benson, had just learned that his 5-year-old daughter had juvenile Batten disease, a rare, fatal, inherited, neurological disorder. The pair had a question for Kingsmore: Could he develop a cheap, reliable genetic test for Batten and other equally horrible diseases, available to all parents to prevent the conception or birth of affected children? Their goal was simple: Do everything possible to eradicate these diseases, because, knowing now which genes cause them, we can. At the time this kind of screening, called carrier testing, was relatively uncommon. Both parents need to carry the same mutated gene for their child to develop a disease like Batten, and many of these recessive diseases are vanishingly rare. The number of affected children born each year can be in the single digits. Given that, it hasn't made fiscal sense to offer tests for dozens of diseases to everyone when so few couples will be carriers of any given one. In communities in which certain mutated genes pop up more often, such as Ashkenazi Jews, carrier testing has been common for years and has drastically reduced the number of babies born with diseases like Tay-Sachs. But DNA sequencing technology was moving fast and costs were dropping. What the two men proposed might now be doable, Kingsmore thought. He took on the project. © 2011 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 14877 - Posted: 01.17.2011

By Tina Hesman Saey Standing over Darwin’s grave in Westminster Abbey, Andrew Feinberg had a realization. Feinberg, a genetics researcher at Johns Hopkins University in Baltimore, looked to the left and saw Newton’s grave. Just above Newton is a plaque honoring physicist Paul Dirac, a pioneer of quantum theory. Inherent in quantum theory is the idea of uncertainty in the interaction of subatomic particles. “So I look back at Darwin’s grave and it hits me; there’s nothing like that in biology,” Feinberg says. Nothing that deals with uncertainty. Yet there is uncertainty in biology. Genes that run in families explain only some of the wide variety of physical appearances among people and their susceptibility to diseases. Much uncertainty in what causes these differences remains. But biologists don’t just accept this seeming randomness as a fundamental part of reality. Instead, they are seeking an explanation for unknown sources of variation in heritable traits, the way physicists are searching for a mysterious substance dubbed dark matter that could explain puzzling aspects of the cosmos. And biologists have proposed some solutions. Feinberg’s, scribbled down at a pub in the shadow of the Tower of London, is that chemical modifications to DNA could be the genetic dark matter. Feinberg is in the minority, though; others have their own favorite theories about what the missing ingredient might be. Some think that researchers just need to hunt harder and longer for common changes in the sequence of genetic letters that make up DNA. But a growing number of researchers are turning to rare genetic changes or absent or duplicated chunks of DNA as important contributors. Others say that interactions among genes deserve more attention. © Society for Science & the Public 2000 - 2010

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 14735 - Posted: 12.04.2010

by Bob Holmes, Eugene, Oregon EXTROVERTS are born not made - or at least, that's what they say. But what if it's more subtle than that? What if we tailor our personalities to our surroundings to make the most of our genes? Conventional comparisons between identical and fraternal twins indicate that nearly half of individual differences in personality traits have some underlying genetic cause. So people have tended to think of personality traits as largely determined by genes, says evolutionary psychologist Aaron Lukaszewski of the University of California at Santa Barbara. He felt there was a flaw in this thinking: if personality were rigidly determined, individuals could end up with the "wrong" personality type for their circumstances. Being extrovert, for instance, exposes people to social conflict. Wimpy men are more likely to suffer in such encounters, while hunkier men may benefit from putting good genes on display. To avoid mismatches, Lukaszewski reasoned, evolution must have favoured a more flexible system. To test this idea, he measured the strength of 85 male and 89 female students and asked them to rate their own attractiveness relative to their peers. Then he gave each a standard personality test to measure how extrovert they were. Sure enough, stronger and more attractive men, and more attractive women, were more extrovert, Lukaszewski reported at a June meeting of the Human Behavior and Evolution Society in Eugene, Oregon. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 14230 - Posted: 07.06.2010

Greg Miller Michael Meaney and Moshe Szyf work in the same Canadian city, but it took a chance meeting at a Spanish pub more than 15 years ago to jump-start a collaboration that helped create a new discipline. Meaney, a neuroscientist at the Douglas Mental Health University Institute in Montreal, studies how early life experiences shape behavior later in life. Across town at McGill University, Szyf is a leading expert on chemical alterations to DNA that affect gene activity. Sometime in the mid-1990s, both men attended the same meeting in Madrid and ended up at a bar talking and drinking beer. "A lot of it," Szyf recalls. Meaney told Szyf about his findings that rat pups raised by inattentive mothers tend to be more anxious as adults than pups raised by more nurturing mothers. He also described how the activity of stress-related genes was altered in the undernurtured pups. At some point in the conversation, Szyf had a flash of insight: This difference must be due to DNA methylation—the chemical alteration he had been studying in stem cells and tumor cells. The idea cut against the conventional thinking in both fields. In neuroscience, the prevailing wisdom held that long-term changes in behavior result from physical changes in neural circuits—such as when neurons build new synapses and become more sensitive to messages from their neighbors. And most scientists who studied DNA methylation thought the process was restricted to embryonic development or cancer cells. © 2010 American Association for the Advancement of Science. All Rights Reserved.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 14221 - Posted: 07.03.2010

By NICHOLAS WADE Researchers studying the social behavior of ants have found that a single gene underlies both the aggressive behavior of the ant colony’s soldiers and the food gathering behavior of its foraging caste. The gene is active in soldier ants, particularly in five neurons in the front of their brain, where it generates large amounts of its product, a protein known as PKG. The exact amount of the protein in the ants’ brains is critical to their behavior. Low levels of PKG predispose both castes of ant to foraging; high levels make the soldiers fight and the foraging caste less interested in food gathering, Christophe Lucas and Marla B. Sokolowski report in the current issue of The Proceedings of the National Academy of Sciences. The soldier and foraging castes in the species of ant under study, known as Pheidole pallidula, have their career choices settled in infancy when they start to be fed different diets. The soldiers develop large heads and jaws, and go on to guard the colony and kill invaders. The foragers, who remain small, specialize in looking for food and bringing back prey to the nest. Copyright 2009 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 12705 - Posted: 06.24.2010

By Jeff Wheelwright Pecos Road runs due west along the southern boundary of Phoenix. On the city side of the road, new subdivisions of retirement homes are pushing up their tile roofs like mushrooms that sprout with no rain. On the other side of the road lies the flat scrub of the Gila River Indian Community, some 600 square miles, most of it empty. The reservation shimmers out of the reach of the builders like a desert mirage. This land was no good to anyone in 1859, when it was allocated to the Pima Indians. Today it has 13,000 Native American residents, living in squat cinder-block houses in scattered, dusty hamlets; three casinos that have boosted the tribal income to $100 million annually from $4 million; irrigated cotton, alfalfa, and citrus, for Pimas were always farmers; and a hospital and two kidney-dialysis clinics, with another medical clinic in the planning stage. Kidney failure is a deadly complication of diabetes, and Pimas, so far as scientists can tell, have the world’s highest rate of type 2 diabetes. The Pimas have grown to hate this superlative perhaps more than the disease itself. Mary Thomas, the 60-year-old ex-governor of the tribe and presently its lieutenant governor, drove me around the community. A few miles south of Pecos Road, we came to the St. Johns Mission, a quiet, whitewashed church. There was once a Catholic boarding school for Indian children on the grounds. Thomas said that when she was 17 and in school here, she went for an eye test and was told she had diabetes. © 2004 The Walt Disney Company. All rights reserved

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 7226 - Posted: 06.24.2010