Links for Keyword: Neurotoxins

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By Elizabeth Pennisi It’s not such a stretch to think that humans can catch the Ebola virus from monkeys and the flu virus from pigs. After all, they are all mammals with fundamentally similar physiologies. But now researchers have discovered that even a virus found in the lowly algae can make mammals its home. The invader doesn’t make people or mice sick, but it does seem to slow specific brain activities. The virus, called ATCV-1, showed up in human brain tissue several years ago, but at the time researchers could not be sure whether it had entered the tissue before or after the people died. Then, it showed up again in a survey of microbes and viruses in the throats of people with psychiatric disease. Pediatric infectious disease expert Robert Yolken from Johns Hopkins University School of Medicine in Baltimore, Maryland, and his colleagues were trying to see if pathogens play a role in these conditions. At first, they didn't know what ATCV-1 was, but a database search revealed its identity as a virus that typically infects a species of green algae found in lakes and rivers. The researchers wanted to find out if the virus was in healthy people as well as sick people. They checked for it in 92 healthy people participating in a study of cognitive function and found it in 43% of them. What’s more, those infected with the virus performed 10% worse than uninfected people on tests requiring visual processing. They were slower in drawing a line connecting a sequence of numbers randomly placed on a page, for example. And they seemed to have shorter attention spans, the researchers report online today in the Proceedings of the National Academy of Sciences. The effects were modest, but significant. © 2014 American Association for the Advancement of Science

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: 20258 - Posted: 10.29.2014

By Jules Wellinghoff A simple change in electric charge may make the difference between someone getting the medicine they need and a trip to the emergency room—at least if a new study bears out. Researchers investigating the toxicity of particles designed to ferry drugs inside the body have found that carriers with a positive charge on their surface appear to cause damage if they reach the brain. These particles, called micelles, are one type of a class of materials known as nanoparticles. By varying properties such as charge, composition, and attached surface molecules, researchers can design nanoparticles to deliver medicine to specific body regions and cell types—and even to carry medicine into cells. This ability allows drugs to directly target locations they would otherwise be unable to, such as the heart of tumors. Researchers are also looking at nanoparticles as a way to transport drugs across the blood-brain barrier, a wall of tightly connected cells that keeps most medication out of the brain. Just how safe nanoparticles in the brain are, however, remains unclear. So Kristina Bram Knudsen, a toxicologist at the National Research Centre for the Working Environment in Copenhagen, and colleagues tested two types of micelles, which were made from different polymers that gave the micelles either a positive or negative surface charge. They injected both versions, empty of drugs, into the brains of rats, and 1 week later they checked for damage. Three out of the five rats injected with the positively charged micelles developed brain lesions. The rats injected with the negatively charged micelles or a saline control solution did not suffer any observable harm from the injections, the team will report in an upcoming issue of Nanotoxicology. © 2014 American Association for the Advancement of Science

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: 19819 - Posted: 07.12.2014

A toxic caffeine level was found in the system of a high school student who died unexpectedly, says a U.S. coroner who warns young people need to be educated about the dangers of taking the potent powder that is sold online. Logan Stiner, 18, was found dead at his family’s home in May. Steiner was an excellent student and a healthy young man who didn’t do drugs, Dr. Stephen Evans, a coroner in Lorain County, Ohio, said Monday. "We sent his blood out for levels, and [when] it came back it was a toxic level. Caffeine toxicity will do exactly what happened to him. It'll lead to things like cardiac arrhytmias and seizures," Evans said in an interview. Use of caffeine from coffee, tea and other beverages is so widespread that it is considered innocuous, but that’s not the case when it’s taken in an overdose amount. Powdered caffeine is sold in bulk over the internet. Problems can arise because adding a teaspoon of the caffeine powder to water is the equivalent of 30 cups of coffee. About one-sixteenth of a teaspoon of the powder is equal to about two cups of coffee. Evans said he recognizes that weightlifters will say Stiner should’ve taken the correct amount. "One-sixteenth of a teaspoon. You expect a kid to figure that out?" He suggested that regulators re-consider internet sales of a pound of powdered caffeine to young people. When Evans and his staff reviewed the pathology literature, they found 18 other cases of deaths in the U.S. from caffeine overdoses. Some were suicides and others were accidental, but he suspects the deaths are underreported since few pathologists investigating deaths from seizure and cardiac arrhytmia check caffeine levels. © CBC 2014

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: 19774 - Posted: 07.01.2014

Emotional and behavioral problems show up even with low exposure to lead, and as blood lead levels increase in children, so do the problems, according to research funded by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. The results were published online June 30 in the journal JAMA Pediatrics. “This research focused on lower blood lead levels than most other studies and adds more evidence that there is no safe lead level,” explained NIEHS Health Scientist Administrator Kimberly Gray, Ph.D. “It is important to continue to study lead exposure in children around the world, and to fully understand short-term and long-term behavioral changes across developmental milestones. It is well-documented that lead exposure lowers the IQ of children.” Blood lead concentrations measured in more than 1,300 preschool children in China were associated with increased risk of behavioral and emotional problems, such as being anxious, depressed, or aggressive. The average blood lead level in the children was 6.4 micrograms per deciliter. While many studies to date have examined health effects at or above 10 micrograms per deciliter, this study focused on lower levels. The CDC now uses a reference level of 5 micrograms per deciliter, to identify children with blood lead levels that are much higher than normal, and recommends educating parents on reducing sources of lead in their environment and continued monitoring of blood lead levels.

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: 19773 - Posted: 07.01.2014

James Hamblin Forty-one million IQ points. That’s what Dr. David Bellinger determined Americans have collectively forfeited as a result of exposure to lead, mercury, and organophosphate pesticides. In a 2012 paper published by the National Institutes of Health, Bellinger, a professor of neurology at Harvard Medical School, compared intelligence quotients among children whose mothers had been exposed to these neurotoxins while pregnant to those who had not. Bellinger calculates a total loss of 16.9 million IQ points due to exposure to organophosphates, the most common pesticides used in agriculture. Last month, more research brought concerns about chemical exposure and brain health to a heightened pitch. Philippe Grandjean, Bellinger’s Harvard colleague, and Philip Landrigan, dean for global health at Mount Sinai School of Medicine in Manhattan, announced to some controversy in the pages of a prestigious medical journal that a “silent pandemic” of toxins has been damaging the brains of unborn children. The experts named 12 chemicals—substances found in both the environment and everyday items like furniture and clothing—that they believed to be causing not just lower IQs but ADHD and autism spectrum disorder. Pesticides were among the toxins they identified. “So you recommend that pregnant women eat organic produce?” I asked Grandjean, a Danish-born researcher who travels around the world studying delayed effects of chemical exposure on children. “That’s what I advise people who ask me, yes. It’s the best way of preventing exposure to pesticides.” Grandjean estimates that there are about 45 organophosphate pesticides on the market, and “most have the potential to damage a developing nervous system.” © 2014 by The Atlantic Monthly Group.

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: 19411 - Posted: 03.26.2014

For tobacco hornworms, bad breath might be the key to surviving the night. As their name suggests, these desert-dwelling caterpillars (larvae of the Manduca sexta moth) regularly chomp on nicotine-laced tobacco leaves. Scientists observed that caterpillars feeding on genetically modified, nicotine-free tobacco plants were more likely to disappear during the night than those chowing down on regular tobacco, leading them to suspect that the hornworms might be repurposing the toxic chemical to defend themselves against nocturnal predators like wolf spiders (Camptocosa parallela, pictured above feasting on a larva). The researchers investigated a gene called CYP6B46, which is active in the hornworm’s gut. Turning the gene off resulted in higher nicotine levels in the hornworms’ poop, suggesting that the gene helps the larvae avoid excreting the chemical by pumping it out of their guts and into their blood. The caterpillars had to be exuding the toxic nicotine somehow, so the scientists gave them an insect version of a breathalyzer test and discovered that they breathe it out with every exhale, the team reports online today in the Proceedings of the National Academy of Sciences. This “toxic halitosis” repelled wolf spiders, which actually flee from caterpillars with nicotine on their breath, as you can see in this video. Still, bad breath is no guarantee of a long life: It didn’t deter some of the hornworms’ other predators, including big-eyed bugs and antlion larvae. © 2013 American Association for the Advancement of Science

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: 19078 - Posted: 12.31.2013

By DANNY HAKIM LONDON — European food regulators said on Tuesday that a class of pesticides linked to the deaths of large numbers of honey bees might also harm human health, and they recommended that the European Commission further restrict their use. The commission, which requested the review, has already taken a tougher stance than regulators in other parts of the world against neonicotinoids, a relatively new nicotine-derived class of pesticide. Earlier this year, some were temporarily banned for use on many flowering crops in Europe that attract honey bees, an action that the pesticides’ makers are opposing in court. Now European Union regulators say the same class of pesticides “may affect the developing human nervous system” of children. They focused on two specific versions of the pesticide, acetamiprid and imidacloprid, saying they were safe to use only in smaller amounts than currently allowed. Imidacloprid was one of the pesticides placed under a two-year ban this year. The review was prompted by a Japanese study that raised similar concerns last year. Imidacloprid is one of the most popular insecticides, and is used in agricultural and consumer products. It was developed by Bayer, the German chemicals giant, and is the active ingredient in products like Bayer Advanced Fruit, Citrus & Vegetable Insect Control, which can be purchased at stores internationally, including Home Depot in the United States. Acetamiprid is sold by Nisso Chemical, a German branch of a Japanese company, though it was developed with Bayer’s help. It is used in consumer products like Ortho Flower, Fruit & Vegetable Insect Killer. The action by European regulators could affect the entire category of neonicotinoid pesticides, however. James Ramsay, a spokesman for the European Food Safety Authority, which conducted the review, said the agency was recommending a mandatory submission of studies related to developmental neurotoxicity “as part of the authorization process in the E.U.” © 2013 The New York Times Company

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: 19048 - Posted: 12.18.2013

By HELENE STAPINSKI IN an office of the American Museum of Natural History, a team of scientists, artists and multimedia experts were discussing what had poisoned Skippy, a cute Jack Russell terrier that had keeled over sick in his virtual backyard. Was it the chocolate he found in the garbage can? Did a snake, or a black widow spider, bite him? Or was a poisonous cane toad to blame? Skippy is just one of many victims in the museum’s show, “The Power of Poison,” opening Nov. 16, to which the staff was busy applying finishing touches. Using iPads, visitors can examine the circumstances surrounding Skippy’s fictional poisoning and, controlling their experience individually, take a crack at solving the mystery. But because the museum is popular with small children, Skippy does not die. Instead, his animated eyes turn into Xs, he runs erratically around the yard, he drools and he vomits a bit. Eventually, though, Skippy rallies to full health. “We were not going to make this a scary show,” said the exhibit’s curator, Dr. Mark Siddall. “Instead you walk out saying, ‘Wow. That was cool.’ ” Dr. Siddall spent two hours enthusiastically discussing poison and its properties at the museum recently, walking through some of the show’s highlights. The exhibit, which takes a look at poison’s role in nature, myth, medicine and human history, examines killer caterpillars, zombie ants and deadly vipers. It also looks at the possible victims, like the heavily slumbering Snow White. Plus the age-old question of what killed Cleopatra. Was it an asp, or something else? And while we’re at it, was Napoleon really poisoned with arsenic? © 2013 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: 18837 - Posted: 10.26.2013

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 BP7e: 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 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: 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 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: 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 BP7e: 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 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: 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 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: 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 BP7e: 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 BP7e: 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 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