Links for Keyword: Neurotoxins

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By DONALD G. McNEIL Jr. Konzo, a disease that comes from eating bitter cassava that has not been prepared properly — that is, soaked for days to break down its natural cyanide — has long been known to cripple children. The name, from the Yaka language of Central Africa, means “tied legs,” and victims stumble as if their knees were bound together. Now researchers have found that children who live where konzo is common but have no obvious physical symptoms may still have mental deficits from the illness. Cassava, also called manioc or tapioca, is eaten by 800 million people around the world and is a staple in Africa, where bitter varieties grow well even in arid regions. When properly soaked and dried, and especially when people have protein in their diet, bitter cassava is “pretty safe,” said Michael J. Boivin, a Michigan State psychiatry professor and lead author of a study published online by Pediatrics. “But in times of war, famine, displacement and hardship, people take shortcuts.” In the Democratic Republic of Congo, Dr. Boivin and colleagues gave tests of mental acuity and dexterity to three groups of children. Two groups were from a village near the Angolan border with regular konzo outbreaks: Half had leg problems; half did not but had cyanide in their urine. The third was from a village 125 miles away with a similar diet but little konzo because residents routinely detoxified cassava before cooking it. © 2013 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Consciousness
Link ID: 18067 - Posted: 04.24.2013

By David Brown, As a bioterrorism agent, ricin has the advantage of being easily made and highly potent. But there have been few fatal cases in the past 50 years, and there is little precise information about the substance’s effects on human beings. Ricin is not a microbe. It does not grow inside the body and can’t be passed from person to person. It is a toxin produced by the castor bean plant. When the beans are crushed for oil, the compound is left behind in the mashed material, of which more than a million tons is produced around the world each year. “It is a plant that grows wild throughout much of North America. You can buy the seeds online,” said Jennifer A. Oakes, a physician and expert in ricin poisoning at Albany Medical College. “It doesn’t take much to get a fatal dose. Somebody could do this in their house if they are motivated to.” Ricin’s best-known victim is Georgi Markov, a Bulgarian journalist who was stabbed by an umbrella on a London street in 1978. The umbrella’s tip injected a tiny metal capsule containing ricin into Markov’s leg. He died three days later. Apart from him, the only other ricin fatalities in the past 50 years have been a few suicides and accidental poisonings, usually after castor beans were eaten but at least once by injecting a crude extract. A person needs to take about 1,000 times as much ricin by mouth as by other routes to get a fatal dose. Unlike nerve agents and botulinum toxin, which disrupt nerve transmission and can cause death in minutes, ricin acts slowly. It stops the synthesis of proteins in cells, killing them over hours or days. A person dies of multi-organ failure as cells break down and fluid and essential electrolytes are lost. © 1996-2013 The Washington Post

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18043 - Posted: 04.18.2013

By Lisa Raffensperger Among the many unpleasant side effects of chemotherapy treatment, researchers have just confirmed another: chemo brain. The term refers to the mental fog that chemotherapy patients report feeling during and after treatment. According to Jame Abraham, a professor at West Virginia University, about a quarter of patients undergoing chemotherapy have trouble focusing, processing numbers, and using short-term memory. A recent study points to the cause. The study relied on PET (positron emission tomography) brain scanning to examine brain blood flow, a marker for brain activity. Abraham and colleagues scanned the brains of 128 breast cancer patients before chemotherapy began and then 6 months later. The results showed a significant decrease in activity in regions responsible for memory, attention, planning and prioritizing. The findings aren’t immediately useful for treating or preventing the condition of chemo brain, but the hard and fast evidence may comfort those experiencing chemo-related forgetfulness. And luckily chemo brain is almost always temporary: patients’ mental processing generally returns to normal within a year or two after chemotherapy treatment ends.

Related chapters from BN8e: 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: 17643 - Posted: 12.29.2012

By Brett Israel and Environmental Health News A widely used pesticide – banned in homes but still commonly used on farms – appears to harm boys’ developing brains more than girls’, according to a new study of children in New York City. In boys, exposure to chlorpyrifos in the womb was associated with lower scores on short-term memory tests compared with girls exposed to similar amounts. The study is the first to find gender differences in how the insecticide harms prenatal development. Scientists say the finding adds to evidence that boys’ brains may be more vulnerable to some chemical exposures. “This suggests that the harmful effects of chlorpyrifos are stronger among boys, which indicates that perhaps boys are more vulnerable to this type of exposure,” said Virginia Rauh, a perinatal epidemiologist at Columbia University and co-author of the study published in July. Chlorpyrifos is an organophosphate insecticide, a powerful class of pesticide that has toxic effects on nervous systems. It was widely used in homes and yards to kill cockroaches and other insects, but in 2001 the U.S. Environmental Protection Agency banned its residential use because of health risks to children. Since then, levels inside U.S. homes have dropped [PDF], but residue remains in many homes. In addition, many developing countries still use the pesticide indoors. Known by the Dow trade name Lorsban, chlorpyrifos is still sprayed on some crops, including fruit trees and vegetables, and also is used on golf courses and for mosquito control. About 10 million pounds of chlorpyrifos are applied to agricultural fields annually, according to the EPA. © 2012 Scientific American,

Related chapters from BN8e: Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 13: Memory, Learning, and Development
Link ID: 17186 - Posted: 08.22.2012

By Janet Raloff A resin in the most commonly used white composite dental fillings may be linked to subtle neuropsychological deficits in children. The association appears in reanalyzed data collected from 434 children as part of a trial begun roughly a decade ago. The original study was designed to probe for IQ or other neurobehavioral impacts of the mercury that can be released by metal-amalgam dental fillings. Half of the kids received amalgam fillings for cavities in back teeth, the rest got composite back fillings. Cavities in front teeth always got composite fillings. Wherever composites were used, baby teeth got a urethane-based resin, while permanent teeth got a resin called bis-GMA that is derived from bisphenol A, or BPA. BPA can mimic the hormonal activity of estrogen and exposure in the womb has been linked to behavioral changes in mice and young children. The 6- to 10-year olds were then followed for five years, with the children or their parents periodically participating in assessments of a kid’s mood, behaviors (including aggression), attitudes at school and interpersonal relationships. That original study, published in 2006, turned up no problems associated with metal fillings. But the research did hint that composite fillings might be worrisome. After reanalyzing their data, the researchers now find that children receiving bis-GMA fillings did exhibit low-level changes on behavioral assessments. © Society for Science & the Public 2000 - 2012

Related chapters from BN8e: 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: 17049 - Posted: 07.17.2012

By Laura Sanders Instead of the indiscriminate destruction of the atom bomb or napalm, the signature weapon of future wars may be precise, unprecedented control over the human brain. As global conflicts become murkier, technologies based on infiltrating brains may soon enter countries’ arsenals, neuroethicists claim in a paper published online October 31 in Synesis. Such “neuroweapons” have the capacity to profoundly change the way war is fought. Advances in understanding the brain’s inner workings could lead to a pill that makes prisoners talk, deadly toxins that can shut down brain function in minutes, or supersoldiers who rely on brain chips to quickly lock in on an enemy’s location. The breadth of brain-based technologies is wide, and includes the traditional psychological tactics used in earlier wars. But the capacity of the emerging technologies is vastly wider — and may make it possible to coerce enemy minds with exquisite precision. In the paper, neuroscientists James Giordano of the Potomac Institute for Policy Studies in Arlington, Va., and Rachel Wurzman of Georgetown University Medical Center in Washington, D.C., describe emerging brain technologies and argue that the United States must be proactive in neuroscience-based research that could be used for national intelligence and security. “A number of these different approaches are heating up in the crucible of possibility, so that’s really increased some of the momentum and the potential of what this stuff can do,” Giordano says. © Society for Science & the Public 2000 - 2011

Related chapters from BN8e: 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: 16024 - Posted: 11.12.2011

By James Gallagher Health reporter, BBC News The idea of making brain cancers glow to help surgeons operate is being tested in the UK. Patients will be given a drug, 5-amino-levulinic acid (5-ALA), which causes a build-up of fluorescent chemicals in the tumour. The theory is that the pink glow will clearly mark the edges of the tumour, making it easier to ensure all of it is removed. More than 60 patients with glioblastoma will take part in the trial. They have cancerous glial cells, which normally hold the brain's nerves cells in place. On average patients survive 15 months after being diagnosed. No room for error In some cancers, such as those of the colon, some of the surrounding tissue can be removed as well as the tumour. Removing a brain tumour needs to be more precise. Dr Colin Watts, who is leading the trial at the University of Cambridge, told the BBC that surgeons "don't want to take too much functional tissue away". BBC © 2011

Related chapters from BN8e: Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior
Link ID: 15967 - Posted: 11.01.2011

by Daniel Strain Agatha Christie, meet your tiniest villain yet: the African crested rat (Lophiomys imhausi). Dogs that try to grab a bite of this spiky-haired East African rodent, more closely related to lemmings or voles than true street rats, often wind up violently ill or even dead. Now, scientists have discovered the secret to the crested rat's fatal kiss: A poison once used by African hunters to kill elephants. When cornered, crested rats don't run or hide like a normal rodent. Instead, they twist to the side and arch their backs, parting their long, gray outer coats, to reveal black-and-white bands that run like racing stripes down their flanks. Like a hornet's yellow-and-black rear or a rattlesnake's rattle, these stripes seem to tell predators one thing: Back off. The rats' defensive postures are fearsome, but they don't explain the trails of sick dogs left in their wakes. Researchers suspected that the rodents were harboring poison, but they didn't know how. In the new study, Fritz Vollrath, an evolutionary biologist at the University of Oxford in the United Kingdom, and colleagues have turned Miss Marple and solved the mystery. Crested rats, it turns out, don't make their own poison; they gather it. The team's first clue was observing a captive crested rat diligently gnaw on pieces of bark from the African tree Acokanthera schimperi, also called the arrow poison tree. The animal would then "slather" its short hairs in fibrous spit. That bark carries large amounts of ouabain, a chemical that overstimulates heart muscle, similar to the poison curare, commonly obtained from South American plants. East African hunters once boiled down the bark to coat poisoned arrows for taking down elephants and other big game. © 2010 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 15645 - Posted: 08.04.2011

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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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 BN8e: 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