Links for Keyword: Neurotoxins

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 110

By CARL ZIMMER The Komodo dragon is already a terrifying beast. Measuring up to 10 feet long, it is the world’s largest lizard. It delivers a devastating bite with its long, serrated teeth, attacking prey as big as water buffaloes. But in a provocative paper to be published this week, an international team of scientists argues that the Komodo dragon is even more impressive. They claim that the lizards use a potent venom to bring down their victims. Other biologists have greeted the notion of giant venomous lizards with mixed reactions. Some think the scientists have made a compelling case, while others say the evidence is thin. Biologists have long been intrigued by the success Komodo dragons have at killing big prey. They use an unusual strategy to hunt, lying in ambush and then suddenly delivering a single deep bite, often to the leg or the belly. Sometimes the victim immediately falls, and the lizards can finish it off. But sometimes a bitten animal escapes. Biologists have noted that the lizard’s victims may collapse later, becoming still and quiet, and even die. For decades, many scientists have speculated that the dragons infected their victims with deadly bacteria that lived in the bits of carrion stuck in their teeth. Yet others have always been skeptical of the bacteria hypothesis. “Your average lion has a much dirtier bite,” said Bryan Fry, a biologist at the University of Melbourne. “It’s complete voodoo.” Copyright 2009 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 12868 - Posted: 06.24.2010

LAURA NELSON Jon-Paul Bingham fumbles around for a condom. Big Bertha is waiting. There’s an awkward pause. “It has to be the non-lubricated kind,” he says. Bingham rips open the packet and slips the prophylactic over a small plastic test tube. Big Bertha is one of Bingham’s nine tropical marine cone snails. These colourful creatures are some of the most venomous beasts on the planet. But the powerful poisons they produce can, in tiny doses, help to reveal how nerve cells function — and potentially help to treat conditions from chronic pain to epilepsy. Currently, most neuroscientists obtain their cone snail toxins from dead animals taken from the wild. But Bingham, a biochemist at Clarkson University in upstate New York, believes that the future lies with cone snail farming. Not only might it help conserve wild populations, he says, but it can also yield a wider range of useful toxins. ‘Milking’ the live snails is a hazardous business. One false move and Bingham could be dead in half an hour. Using forceps, he dangles a dead goldfish, the same length as Big Bertha, in front of her. Behind the bait, the condom is stretched over the mouth of the plastic tube. © Nature News Service / Macmillan Magazines Ltd 2004

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 5737 - Posted: 06.24.2010

Tiny particles enter the brain after being inhaled. JIM GILES Nanoparticles - tiny lumps of matter that could one day to be used to build faster computer circuits and improve drug delivery systems - can travel to the brain after being inhaled, according to researchers from the United States1. The finding sounds a cautionary note for advocates of nanotechnology, but may also lead to a fuller understanding of the health effects of the nanosized particles produced by diesel engines. Günter Oberdörster of the University of Rochester in New York and colleagues tracked the progress of carbon particles that were only 35 nanometres in diameter and had been inhaled by rats. In the olfactory bulb - an area of the brain that deals with smell - nanoparticles were detected a day after inhalation, and levels continued to rise until the experiment ended after seven days. © Nature News Service / Macmillan Magazines Ltd 2004

Related chapters from BP7e: Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior
Link ID: 4778 - Posted: 06.24.2010

Nora Schultz There is a cure for zombies after all – if you are a cockroach. A new study has shown that cockroaches that turned into zombies after being stung by a parasitic wasp can be revived with an antidote. Cockroaches can lose their ability to walk when stung by jewel wasps (Ampulex compressa) – the females of which use the cockroaches to feed their young. The wasp, being much smaller than the cockroach, has evolved a fine sting that can deliver a venom cocktail directly into the cockroach’s brain. The poisons effectively turn the cockroach into a zombie. The cockroach is not entirely paralysed, but loses its ability to escape. The wasp then grabs it by the antennae and pulls it into its burrow and lays an egg on its abdomen. The cockroach sits still while the wasp's larva hatches, chews a hole into its belly, and slowly eats its living host from the inside over a period of eight days. To find out if he could revive the cockroaches, Frederic Libersat from Ben-Gurion University in Be'er Sheva, Israel, injected stung zombie cockroaches with candidate chemicals that resembled various neurotransmitters in the brain. Journal reference: The Journal of Experimental Biology (vol 210, p 4411) © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 11023 - Posted: 06.24.2010

University of Utah researchers isolated an unusual nerve toxin in an ocean-dwelling snail, and say its ability to glom onto the brain's nicotine receptors may be useful for designing new drugs to treat a variety of psychiatric and brain diseases. "We discovered a new toxin from a venomous cone snail that may enable scientists to more effectively develop medications for a wide range of nervous system disorders including Parkinson's disease, Alzheimer's disease, depression, nicotine addiction and perhaps even schizophrenia," says J. Michael McIntosh. Discovery of the new cone snail toxin will be published Friday, Aug. 25 in The Journal of Biological Chemistry by a team led by McIntosh, a University of Utah research professor of biology, professor and research director of psychiatry, member of the Center for Peptide Neuropharmacology and member of The Brain Institute. McIntosh is the same University of Utah researcher who – as an incoming freshman student in 1979 – discovered another "conotoxin" that was developed into Prialt, a drug injected into fluid surrounding the spinal cord to treat severe pain due to cancer, AIDS, injury, failed back surgery and certain nervous system disorders. Prialt was approved in late 2004 in the United States and was introduced in Europe last month.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 9252 - Posted: 06.24.2010

ST. PAUL, Minn. – Eighteen years later, people who worked with lead have significant loss of brain cells and damage to brain tissue, according to a new study published in the May 23, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology. The study examined 532 former employees of a chemical manufacturing plant who had not been exposed to lead for an average of 18 years. The workers had worked at the plant for an average of more than eight years. The researchers measured the amount of lead accumulated in the workers' bones and used MRI scans to measure the workers' brain volumes and to look for white matter lesions, or small areas of damage in the brain tissue. The higher the workers' lead levels were, the more likely they were to have smaller brain volumes and greater amounts of brain damage. A total of 36 percent of the participants had white matter lesions. Those with the highest levels of lead were more than twice as likely to have brain damage as those with the lowest lead levels. Those with the highest levels of lead had brain volumes 1.1 percent smaller than those with the lowest lead levels. "The effect of the lead exposure was equivalent to what would be expected for five years of aging,"said study author Walter F. Stewart, PhD.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 8949 - Posted: 06.24.2010

Durham, N.C. -– Duke University Medical Center researchers have found that the naturally occurring marine toxin domoic acid can cause subtle but lasting cognitive damage in rats exposed to the chemical before birth. Humans can become poisoned by the potentially lethal, algal toxin after eating contaminated shellfish. The researchers saw behavioral effects of the toxin in animals after prenatal exposure to domoic acid levels below those generally deemed safe for adults, said Edward Levin, Ph.D. Those effects –- including an increased susceptibility to disruptions of memory -- persisted into adulthood, he said. The findings in rats, therefore, imply that the toxin might negatively affect unborn children at levels that do not cause symptoms in expectant mothers, said Levin. While the researchers note that eating seafood offers significant health benefits, they said their findings suggest that the current threshold of toxin at which affected fisheries are closed should perhaps be lowered. The Federal Drug Administration (FDA) set the current limit based on levels safe for adults, Levin said. "A single administration of domoic acid to pregnant rats had a lasting affect on the performance of their offspring as adults," Levin said. "The consequences are life-long. "The findings suggest we may need to re-evaluate monitoring of waters, shellfish and fish to make sure that the most sensitive parts of the human population are protected from toxic exposure to domoic acid," he continued. © 2001-2005 Duke University Medical Center

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 7859 - Posted: 06.24.2010

Researchers have long known that mercury increases mortality and decreases fertility in fish, but the underlying metabolic processes are still unknown. New research posted on the ES&T Research ASAP website (es0483490) helps uncover some of the mystery by examining which genes respond when fish are fed methylmercury (MeHg). Although multiple genes turn on in the muscle and liver to help store and detoxify the metal, the brain appears unresponsive and accumulates high levels of mercury. This leads researchers to believe that neural tissue might be unable to defend itself against this toxic compound. The brains of zebrafish fail to mount a defense against methylmercury. "It was a big surprise when we found that genes in the neural system were not responding," says study author Jean-Paul Bourdineaud, a professor of biochemistry at the University of Bordeaux (France). Previous research has shown that mercury can cause lesions in the brain, and a recent study found that MeHg can decrease the density of neurotransmitters in otters that consume diets heavy in fish contaminated with MeHg. (Environ. Sci. Technol. 2005, 39, 218A) The zebra fish in the study were fed diets that contain MeHg at concentrations similar to those found in wild fish (Environ. Sci. Technol. 2002, 36, 877–883). Thirteen different genes were then tested in liver, muscle, and brain tissue. These genes encode for proteins known to be involved in different functions such as antioxidant defense, metal chelation, DNA repair, and cell death. "Testing this range of genes gives us a toxicological survey of mercury's effects," says Bourdineaud. Copyright © 2005 American Chemical Society

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 7258 - Posted: 06.24.2010

The red Mozambique spitting cobra stiffens, fixing its gaze on the victim's face, which is moving backwards and forwards in front of it. For several seconds it remains erect like this; then its head flashes forwards. For an instant the fangs in front of its pale pink throat are visible in its wide-open mouth, as they squirt the venom at high pressure towards the victim. On the plastic visor two red spiral patterns appear. The eyes behind it look surprisingly unperturbed. "I sprayed the visor beforehand with rhodamine," Katja Tzschätzsch calmly explains, "It's a pigment which dyes liquids red. This makes the traces of venom easier to see." In her undergraduate dissertation the trainee teacher investigated what spitting cobras aim at when spitting. "In the literature it often says: they aim at the eyes," her supervisor Dr. Guido Westhoff, junior lecturer in Professor Horst Bleckmann's team, explains. "However, up to now nobody has investigated it." The cocktail of toxins partly consists of nerve poisons, but also contains components which are harmful to tissue. Through a narrow channel in their fangs the snakes can spray the liquid at high pressure – similar to a bullet in the barrel of a gun. If they manage to hit an eye, the sensitive cornea reacts with severe stinging pain. In the worst case these burns can ultimately lead to blindness.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 6845 - Posted: 06.24.2010

Although recent reports on mercury have focused on the dangers to humans, some researchers feel that public health could be better guarded if standards were enforced that protect wildlife. Gary Heinz, a research biologist with the U.S. Geological Survey (USGS) at the Patuxent Wildlife Research Center in Laurel, Md., has found that some bird species are much more sensitive than humans to mercury. “To a large extent, researchers in human toxicology ignore the work that is being done in wildlife toxicology,” he says. “The reverse is also unfortunately true.” Human dietary guidelines for mercury range from a high of 1.0 parts per million (ppm) in the United States to a low of 0.4 ppm in Japan. However, birds can show ill effects at much lower dietary concentrations than humans. Mallard ducks, for instance, experience harmful influences to eggs when fed as little as 0.1 ppm of methylmercury, and ring-necked pheasant show effects at 0.2 ppm. Yet, only four species of birds have been well studied, because captive breeding experiments with wild animals are both daunting and expensive, say USGS researchers. Heinz has used direct injection of methylmercury into eggs as a quick and effective means to test chick mortality in 20 bird species. While mallards have increased chick mortality at 0.8–1.0 ppm, the most sensitive species is the white ibis, whose chicks begin dying at methylmercury concentrations of only 0.1 ppm. He also notes that these are mercury levels that birds are likely to encounter in the wild. Copyright © 2004 American Chemical Society

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 6421 - Posted: 06.24.2010

DALLAS – – UT Southwestern Medical Center at Dallas researchers have uncovered damage in a specific, primitive portion of the nervous systems of veterans suffering from Gulf War syndrome. UT Southwestern researchers report that damage to the parasympathetic nervous system may account for nearly half of the typical symptoms – including gallbladder disease, unrefreshing sleep, depression, joint pain, chronic diarrhea and sexual dysfunction – that afflict those with Gulf War syndrome. Their findings will be published in the October issue of the American Journal of Medicine and are currently available online. "The high rate of gallbladder disease in these men, reported in a previous study, is particularly disturbing because typically women over 40 get this. It's singularly rare in young men," said Dr. Robert Haley, chief of epidemiology at UT Southwestern and lead author of the new study. The parasympathetic system regulates primitive, automatic bodily functions such as digestion and sleep, while the sympathetic nervous system controls the "fight or flight" instinct.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 6162 - Posted: 06.24.2010

(Philadelphia, PA) – Later this fall, emergency-medicine physicians enter into what they call the "CO season" – a time when faulty furnaces and other mechanical mishaps lead to a spike in cases of carbon monoxide (CO) poisoning. CO poisoning is the leading cause of injury and death by poisoning worldwide, with about 40,000 people treated in the U.S. annually. Brain damage occurs – days to weeks later – in half of the patients with a serious case of CO poisoning. The physiological causes of this delayed decline were not well understood until now. A team led by Stephen R. Thom, MD, PhD, Professor of Emergency Medicine and Chief of Hyperbaric Medicine, at the University of Pennsylvania School of Medicine, report this week online in the Proceedings of the National Academies of Sciences, that CO causes profound changes in myelin basic protein (MBP) – a major protein constituent of myelin, the protective sheath surrounding neurons. Using an animal model, they showed that the CO-induced changes in MBP set into motion an autoimmune response in which lymphocytes, triggered to eliminate altered MBP, continue to attack normal MBP. Specifically, the researchers found that by-products of CO metabolism in the brain alter the charge and structure of MBP. "These changes in MBP have also been demonstrated in multiple sclerosis, which is why we paralleled the study along those lines," says Thom.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 6062 - Posted: 06.24.2010

HELEN PEARSON
A cell door that automatically snaps shut in milliseconds - this isn't the latest jailbreak deterrent but a fundamental part of our cells. Nearly 50 years after this microscopic marvel was discovered, researchers in New York have dissected the inner workings of the molecule responsible for generating the body's electrical impulses1. All excitable cells - such as those responsible for nerve signals, muscle contraction or the heart beat - depend on ion channels in the cell membrane. Triggered to open by a small voltage, such channels let through a flood of electrically charged ions, then promptly slam shut. The 'ball-and-chain' model was put forward in the 1970s to explain how this 'inactivation' occurs. The model suggested that a plug - or ball - swinging on a molecular 'chain' on the inside of the channel stops up the opening. Now Roderick MacKinnon and his colleagues at Rockefeller University in New York have found that the ball is more like a snake that sneaks inside the channel to block it. 1.Zhou, M., Morais-Cabral, J. H., Mann, S. & MacKinnon, R. Potassium channel receptor site for the inactivation gate and quaternary amine inhibitors. Nature 411, 657–661 (2001). © Macmillan Magazines Ltd 2001 - NATURE NEWS SERVICE Nature © Macmillan Publishers Ltd 2001 Reg. No. 785998 England.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 300 - Posted: 06.24.2010

By Katherine Harmon Even cobras need to defend themselves sometimes. These venomous snakes keep adversaries at bay by spitting a neurotoxin or other substance into their perceived enemy's eyes, causing severe pain and sometimes blindness. And they are incredibly accurate in hitting their target—even though it is often moving and more than a meter away. But how can a cobra be so adept at adjusting its venom trajectory (usually launched straight from openings in the fangs) to different scenarios, when fang and venom-opening sizes remain the same? "Basic fluid dynamics would lead you to think that the pattern of the fluid should be fixed," Bruce Young, of the Department of Physical Therapy at the University of Massachusetts Lowell and co-author of a new study, said in a prepared statement. To find out, Young and his colleagues headed into the snake-filled labs of Horst Bleckmann at the University of Bonn Institute of Zoology to taunt some cobras. After donning proper protection, Young met his experimental partners: red spitting cobras (Naja pallida), black-necked spitting cobras (Naja nigricollis) and black-and-white spiting cobras (Naja siamensis). "I just put on the goggles and the cobras start spitting all over," Young said. He was also outfitted with accelerometers on his head, and his human colleagues used high-speed video to film cobras spitting and then compared the movements of the two. The results were published online May 14 in The Journal of Experimental Biology. © 2010 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 14073 - Posted: 06.24.2010

By Janet Raloff When Lilian Calderón-Garcidueñas recruited children for a study probing the effects of air pollution, Ana was just 7. The trim girl with an above-average IQ of 113 “was bright, very beautiful and clinically healthy,” the physician and toxicologist recalls. But now Ana (not her real name) is 11. And after putting her and 54 other children from a middle-class area of Mexico City through a new battery of medical and cognitive tests, Calderón-Garcidueñas found that something has been ravaging the youngsters’ lungs, hearts — and, especially troubling, their minds. Brain scans and screening for chemical biomarkers in the blood pointed to inflammation affecting all parts of the brain, says Calderón-Garcidueñas, of the National Institute of Pediatrics in Mexico City and the University of Montana in Missoula. On MRI scans, white spots showed up in the prefrontal cortex. In the elderly, she says, such brain lesions tend to denote reduced blood flow and often show up in people who are developing dementias, including Alzheimer’s disease. In autopsies of seemingly healthy Mexico City children who had died in auto accidents or other traumatic events, Calderón-Garcidueñas uncovered brain deposits of amyloid-beta and alpha-synuclein, proteins that serve as hallmarks of Alzheimer’s and Parkinson’s diseases. Several years earlier, she had found similar abnormalities in homeless Mexico City dogs and exaggerated versions of the abnormalities in local 20- to 50-year-olds. © Society for Science & the Public 2000 - 2010

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 14059 - Posted: 06.24.2010

By Laura Sanders When the monitor lizard chomped into Bryan Fry, it did more than turn his hand into a bloody mess. Besides ripping skin and severing tendons, the lizard delivered noxious venom into Fry’s body, injecting molecules that quickly thinned his blood and dilated his vessels. As the tiny toxic assassins dispersed throughout his circulatory system, they hit their targets with speed and precision, ultimately causing more blood to gush from Fry’s wound. Over millions of years, evolution has meticulously shaped these toxins into powerful weapons, and Fry was feeling the devastating consequences firsthand. “I’ve never seen arterial bleeding before, and I really don’t want to ever see it again. Especially coming out of my own arm,” says Fry, a venom researcher at the University of Melbourne in Australia. To unlock the molecular secrets of venom, Fry and other researchers have pioneered a burgeoning field called venomics. With cutting-edge methods, the scientists are teasing apart and cataloging venom’s ingredients, some of which can paralyze muscles, make blood pressure plummet or induce seizures by scrambling brain signals. Researchers are also learning more about how these toxins work. Discovering venom’s tricks may allow scientists to rehabilitate these damaging molecules and convert them from destroyers to healers. Venom might be teeming with wonder drugs, for instance. After all, a perfect venom toxin works with lightning speed, remains stable for a long time and strikes its mark with surgical exactitude — attributes that drugmakers dream about. © Society for Science & the Public 2000 - 2009

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 13116 - Posted: 06.24.2010

By Janet Raloff Testing for lead only in infants and toddlers may be a mistake, a new study suggests. Pediatricians routinely test very young children because this is the age when blood concentrations of the neurotoxic heavy metal tend to be highest. But older children can face significant lead exposures, and lead’s ability to lower IQ, the new study shows, is much greater for exposures in early school-age children than in toddlers. The study, which will appear in an upcoming Environmental Health Perspectives, also finds that the later childhood exposures correlate more strongly than earlier ones with an exaggerated risk of incurring future criminal arrests for violent behavior. The new data “get at a key concept in environmental health: that there may be some windows of vulnerability — stages of development — that are more vulnerable than others,” notes environmental epidemiologist Howard Hu of the University of Michigan in Ann Arbor. If school-age brains are more susceptible to lead toxicity than younger ones, “that’s important to know, from a public health perspective,” he says. Looking for lead in older children would be a first step in identifying families that need counseling on reducing sources of lead in and around the home. Richard Hornung and his colleagues at Cincinnati Children’s Hospital Medical Center analyzed data on lead levels and IQ from 462 children. About half of the data were collected from kids in Cincinnati during the early 1980s, the rest from kids in Rochester, N.Y., during the mid-1990s. © Society for Science & the Public 2000 - 2009

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 12859 - Posted: 06.24.2010

By JASCHA HOFFMAN Has the Clean Air Act done more to fight crime than any other policy in American history? That is the claim of a new environmental theory of criminal behavior. In the early 1990s, a surge in the number of teenagers threatened a crime wave of unprecedented proportions. But to the surprise of some experts, crime fell steadily instead. Many explanations have been offered in hindsight, including economic growth, the expansion of police forces, the rise of prison populations and the end of the crack epidemic. But no one knows exactly why crime declined so steeply. The answer, according to Jessica Wolpaw Reyes, an economist at Amherst College, lies in the cleanup of a toxic chemical that affected nearly everyone in the United States for most of the last century. After moving out of an old townhouse in Boston when her first child was born in 2000, Reyes started looking into the effects of lead poisoning. She learned that even low levels of lead can cause brain damage that makes children less intelligent and, in some cases, more impulsive and aggressive. She also discovered that the main source of lead in the air and water had not been paint but rather leaded gasoline — until it was phased out in the 1970s and ’80s by the Clean Air Act, which took blood levels of lead for all Americans down to a fraction of what they had been. “Putting the two together,” she says, “it seemed that this big change in people’s exposure to lead might have led to some big changes in behavior.” Copyright 2007 The New York Times Company

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: 10864 - Posted: 06.24.2010

Michael Hopkin They say you are what you eat. And that's especially true of Rhabdophis tigrinus — zoologists have discovered that this snake eats poisonous toads and keeps their venom for itself. Rather than going to the trouble of making its own venom to use against predators, R. tigrinus, which is found in Asia, takes the venom from its prey and transports it to its own venom glands for storage and use. The snakes eat a wide range of prey, often including toads that secrete defensive poisons called bufadienolides through their skin. When fed a diet featuring these toads, the snakes' venom glands fill up with an almost chemically identical venom, report Deborah Hutchinson of Old Dominion University in Norfold, Virginia, and her colleagues. Snakes lacking toads in their diet do not gather the poison, the researchers add. Their findings are published in Proceedings of the National Academy of Sciences1. Many invertebrates, such as sea slugs, collect and store toxins from their plant food to make themselves unpalatable to predators. A few species of poisonous frogs also get their toxins from insects in their diet. But examples of vertebrate predators using venom from vertebrate prey are rare, and the only other species known to do it only stores venom temporarily. ©2007 Nature Publishing Group

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 9896 - Posted: 06.24.2010

Scientists supported by the National Institute of Dental and Craniofacial Research (NIDCR), part of the National Institutes of Health, report in this week’s Journal of the American Medical Association the results of the first-ever randomized clinical trials to evaluate the safety of placing amalgam fillings, which contain mercury, in the teeth of children. Both studies — one conducted in Europe, the other in the United States — independently reached the conclusion: Children whose cavities were filled with dental amalgam had no adverse health effects. The findings included no detectable loss of intelligence, memory, coordination, concentration, nerve conduction, or kidney function during the 5-7 years the children were followed. The researchers looked for measurable signs of damage to the brain and kidneys because previous studies with adults indicated these organs might be especially sensitive to mercury. The authors noted that children in both studies who received amalgam, informally known as “silver fillings,” had slightly elevated levels of mercury in their urine. But after several years of analysis, they determined the mercury levels remained low and did not correlate with any symptoms of mercury poisoning. “What’s particularly impressive is the strength of the evidence,” said NIDCR director Dr. Lawrence Tabak. “The studies evaluated mercury exposure in two large, geographically distinct groups of children and reached similar conclusions about the safety of amalgam.”

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 8798 - Posted: 06.24.2010