Links for Keyword: Neurotoxins

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by Kathleen McAuliffe Elijah Stommel, a neurologist at the Dartmouth-Hitchcock medical center in New Hampshire, often has to deliver bad news to his patients, but there is one diagnosis he particularly dreads. Amyotrophic lateral sclerosis, or ALS, kills motor neurons in the brain and spinal cord, progressively paralyzing the body until even swallowing and breathing become impossible. The cause of ALS is unknown. Though of little solace to the afflicted, Stommel used to offer one comforting fact: ALS was rare, randomly striking just two of 100,000 people a year. Then, a couple of years ago, in an effort to gain more insight into the disease, Stommel enlisted students to punch the street addresses of about 200 of his ALS patients into Google Earth. The distribution of cases that emerged on the computer-generated map of New England shocked him. In numbers far higher than national statistics predicted, his current and deceased patients’ homes were clustered around lakes and other bodies of water. The flurry of dots marking their locations was thickest of all around bucolic Mascoma Lake, a rural area just 10 miles from Dartmouth Medical School. About a dozen cases turned up there, the majority diagnosed within the past decade. The pattern did not appear random at all. “I started thinking maybe there was something in the water,” Stommel says. That “something,” he now suspects, could be the environmental toxin beta-methylamino-L-alanine, or BMAA. This compound 
is produced by cyanobacteria, the blue-green algae that live in soil, lakes, and oceans. Cyanobacteria are consumed by fish and other aquatic creatures. Recent studies have found BMAA in seafood, suggesting that certain diets and locations may put people at particular risk. More worrisome, blooms of cyanobacteria are becoming increasingly common, fueling fears that their toxic by-product may be quietly fomenting an upsurge in ALS—and possibly other neurological disorders like Alzheimer’s disease and Parkinson’s as well. © 2011, Kalmbach Publishing Co.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 15598 - Posted: 07.25.2011

By LISA SANDERS, M.D. The Challenge: Can you solve a medical mystery involving a 38-year-old gardener with a leg rash, numbness and chills? The Presenting Problem: A 38-year-old man comes to the emergency room with a rash and numbness and tingling in his right leg. The Patient’s Story: The patient was working in his tiny city garden in Washington one afternoon when he felt a strange burning in his right foot. He took off the plastic garden sandal he was wearing but didn’t see anything under the layer of dark soil that he dusted off his foot. Half an hour later, when he looked at his leg, he noticed a burst of fluorescent purple climbing from his foot, over his ankle and nearly to the knee. On closer inspection, the lines of day-glo violet seemed to trace the veins in his leg. He still had a couple more hours of work to do that day, so rather than stopping, he pulled out his phone and snapped a couple of pictures of his leg. He was a healthy guy and wasn’t particularly worried. But by the end of the day he would be. As the man continued his work, he became aware that the burning sensation he’d felt in his foot was climbing up his leg, well past the knee. Still, he wanted to get the plants cleared and continued working for another couple of hours. Finally, he put away the shovel and other tools, cleared away the plants he’d pulled up and went in to take a shower. Under the hot stream he could see that the fluorescent purple rash had faded but was still visible. His leg now had that combination of numbness and tingling you get when a body part “falls asleep.” He dressed and joined his wife and 8-year-old daughter for a dinner of takeout pizza. © 2011 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: 15554 - Posted: 07.14.2011

By Nadia Drake Indiana Jones, intrepid cinematic archaeologist, is famously afraid of snakes. Perhaps he wouldn’t need to be if he had a new ointment developed by scientists in Australia. Quickly applying a nitric oxide–containing ointment near the bite site slows the spread of some venoms, including the notorious eastern brown snake’s, the researchers report online June 26 in Nature Medicine. “This treatment might make all the difference between dying on the road and getting to the hospital in time,” says physician and emeritus professor of tropical medicine David Warrell of the University of Oxford, who was not involved with the study. Worldwide, snakebite causes approximately 100,000 deaths and 400,000 limb amputations each year. Physiologist Dirk van Helden at the University of Newcastle and his colleagues showed that in humans, applying an ointment containing nitric oxide within one minute of a simulated snakebite slows the transit of injected tracer molecules. Foot-to-groin venom travel times increased from an average of 13 minutes without the ointment to an average of 54 minutes with the ointment applied in a 5-centimeter diameter circle just up the limb from the bite site. The group also tested the effects of the cream on rats injected with venom from the brown snake (Pseudonaja textilis). Its potent venom travels through the body’s lymphatic system, eventually halting respiration and causing death. “It’s particularly nasty, one of the most toxic things in the world,” says van Helden. © Society for Science & the Public 2000 - 2011

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: 15495 - Posted: 06.27.2011

By SHARON LaFRANIERE MENGXI VILLAGE, China — On a chilly evening early last month, a mob of more than 200 people gathered in this tiny eastern China village at the entrance to the Zhejiang Haijiu Battery Factory, a maker of lead-acid batteries for motorcycles and electric bikes. They shouldered through an outer brick wall, swept into the factory office and, in an outpouring of pure fury, smashed the cabinets, desks and computers inside. News had spread that workers and villagers had been poisoned by lead emissions from the factory, which had operated for six years despite flagrant environmental violations. But the truth was even worse: 233 adults and 99 children were ultimately found to have concentrations of lead in their blood, up to seven times the level deemed safe by the Chinese government. One of them was 3-year-old Han Tiantian, who lived just across the road from the plant. Her father, Han Zongyuan, a factory worker, said he learned in March that she had absorbed enough lead to irreversibly diminish her intellectual capacity and harm her nervous system. “At the moment I heard the doctor say that, my heart was shattered,” Mr. Han said in an interview last week. “We wanted this child to have everything. That’s why we worked this hard. That’s why we poisoned ourselves at this factory. Now it turns out the child is poisoned too. I have no words to describe how I feel.” Such scenes of heartbreak and anger have been repeated across China in recent months with the discovery of case after case of mass lead poisoning — together with instances in which local governments tried to cover them up. © 2011 The New York Times Company

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: 15444 - Posted: 06.16.2011

By SEAN B. CARROLL Have you ever tried to think up the worst meal you could imagine? How about blue-ringed octopus, floral egg crab, basket shell snails and puffer fish. Sure, some people may think these are delicacies, and puffer fish is certainly treated as such in parts of Asia. But each dish has something more important in common: they are all deadly. Each of these animals is chock full of a powerful neurotoxin called tetrodotoxin. First isolated from the puffer fish, tetrodotoxin is among the most potent toxins known. It is 100 times as toxic by weight as potassium cyanide — two milligrams can kill an adult human — and it is not destroyed by cooking. Just half an ounce of the fish liver, known as fugu kimo in Japan and eaten by daring connoisseurs, can be lethal. When ingested, the toxin paralyzes nerves and muscles, which leads to respiratory failure and, in some cases each year, death. In 1975, the Kabuki actor Bando Mitsugoro VIII ordered four fugu kimo in a restaurant in Kyoto, claiming he could resist the poison. He was wrong. Tetrodotoxin is found in more than just marine creatures. It is present in high concentrations in the skin of certain newts in North America and Japan, and in several kinds of frogs in Central and South America and Bangladesh. The widespread occurrence of tetrodotoxin poses some intriguing riddles. First, how is it that such different animals, belonging to separate branches of the animal kingdom, have all come to possess the same deadly poison? And how is it that they are able to tolerate high levels of tetrodotoxin while others cannot? 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: 13590 - Posted: 06.24.2010

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. Gnter 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 Tzschtzsch 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 Caldern-Garcidueas 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, Caldern-Garcidueas 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 Caldern-Garcidueas, 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, Caldern-Garcidueas 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