By GRETCHEN REYNOLDS The Morris water maze is the rodent equivalent of an I.Q. test: mice are placed in a tank filled with water dyed an opaque color. Beneath a small area of the surface is a platform, which the mice can’t see. Despite what you’ve heard about rodents and sinking ships, mice hate water; those that blunder upon the platform climb onto it immediately. Scientists have long agreed that a mouse’s spatial memory can be inferred by how quickly the animal finds its way in subsequent dunkings. A “smart” mouse remembers the platform and swims right to it. In the late 1990s, one group of mice at the Salk Institute for Biological Studies, near San Diego, blew away the others in the Morris maze. The difference between the smart mice and those that floundered? Exercise. The brainy mice had running wheels in their cages, and the others didn’t. Scientists have suspected for decades that exercise, particularly regular aerobic exercise, can affect the brain. But they could only speculate as to how. Now an expanding body of research shows that exercise can improve the performance of the brain by boosting memory and cognitive processing speed. Exercise can, in fact, create a stronger, faster brain. This theory emerged from those mouse studies at the Salk Institute. After conducting maze tests, the neuroscientist Fred H. Gage and his colleagues examined brain samples from the mice. Conventional wisdom had long held that animal (and human) brains weren’t malleable: after a brief window early in life, the brain could no longer grow or renew itself. The supply of neurons — the brain cells that enable us to think — was believed to be fixed almost from birth. As the cells died through aging, mental function declined. The damage couldn’t be staved off or repaired. Copyright 2007 The New York Times Company

Keyword: Neurogenesis
Link ID: 10621 - Posted: 06.24.2010

By GINA KOLATA The havoc diabetes wreaks is clear. But researchers are puzzled by many aspects of the disease. Why, for example, are most people with Type 2 diabetes overweight or obese, yet most overweight or obese people do not have diabetes? One clue may lie in the fat cells themselves. The cells release fat and breakdown products of fat — triglycerides and free fatty acids — into the blood. These substances may make cells less able to respond to insulin, increasing the body’s demand for the hormone. Another clue is a paradoxical finding about a hormone, adiponectin, made by fat cells. Adiponectin makes cells more responsive to insulin. “Oddly enough,” said Dr. C. Ronald Kahn, a diabetes researcher and professor of medicine at Harvard Medical School, “the fatter people become, the less adiponectin their fat cells produce.” So one way obesity might increase the risk that a person will develop diabetes is by leading to a release of more fatty acids and a decline in adiponectin. This would lead to more insulin resistance and a demand for more insulin. If that demand cannot be met, the result, eventually, would be diabetes. But figuring out why obesity predisposes some people to diabetes is only part of the puzzle. Researchers also are struggling with a fundamental question. Why does high blood sugar lead to any of the disease’s complications — heart disease, stroke, nerve damage, kidney damage and sight-threatening eye damage? Copyright 2007 The New York Times Company

Keyword: Obesity
Link ID: 10620 - Posted: 06.24.2010

By Paul Raeburn Two years ago Katherine M. Flegal, a re­search­er at the Centers for Disease Control and Prevention, did a new statistical analysis of national survey data on obesity and came to a startling conclusion: mildly overweight adults had a lower risk of dying than those at so-called healthy weights. Decades of research and thousands of studies have suggested precisely the opposite: that being even a little overweight is bad and that being obese is worse. The distinction between overweight and obese—which are sometimes both classified under the rubric of obesity—can be confusing. It relates to the measure called body mass index (BMI), derived by dividing one’s weight in kilograms by the square of one’s height in meters. A myriad of Internet-based calculators will handle the math for you. The only thing to remember is that a BMI of at least 25 but less than 30 is considered overweight, and one of 30 or more is characterized as obese. The long-established conventional wisdom holds that Americans carrying excess fat are at increased risk of death from heart disease, diabetes and various kinds of cancer. And those who do not die of obesity-related ailments can possibly look forward to a variety of other unpleasant consequences of their weight, including diabetes and its complications, such as the loss of an arm or leg, blindness and kidney failure. That has been the consensus view of most experts for decades, and it has not changed. © 1996-2007 Scientific American, Inc

Keyword: Obesity
Link ID: 10619 - Posted: 06.24.2010

By Kristin Leutwyler Ozelli Nora D. Volkow is director of the National Institute of Drug Abuse. Before her appointment in 2003, she held various positions at Brookhaven National Laboratory and also served as professor of psychiatry and associate dean for the medical school at Stony Brook University. In her research, she was first to use imaging technology to investigate neurochemical changes associated with addiction Mounting evidence shows that compulsive eating and drug abuse engage some of the same brain circuits in similar ways, offering a new angle for understanding and treating obesity. In an interview with Scientific American, Nora D. Volkow, director of the National Institute on Drug Abuse and a pioneer in the study of addiction, explains. How do foods and drugs affect the brain in the same way? The system in the brain that both drugs and food activate is basically the circuitry that evolved to reward behaviors that are essential for our survival. One of the reasons why humans are attracted to food is because of its rewarding, pleasurable properties. When we experience pleasure, our brains learn to associate the pleasurable experience with the cues and conditions that predict it. In other words, the brain remembers not just what the food tasted like but also the sensation of pleasure itself, and the cues or behaviors that preceded it. That memory becomes stronger and stronger as the cycle of predicting, seeking and obtaining pleasure becomes more reliable. When you remember that food, you also automatically expect the pleasure that comes from it. So when you like something very much, the mere fact of being re-exposed to it, even if it is out of reach, will trigger the desire to get it. In scientific terms, we call this process conditioning. © 1996-2007 Scientific American, Inc.

Keyword: Obesity; Drug Abuse
Link ID: 10618 - Posted: 06.24.2010

A Swiss woman who fell off her bicycle has yielded a unique insight into how auditory hallucinations are generated. The woman suffered damage to the part of the brain where speech is generated and could speak only in short, stunted words and sentences. Five months later, when she suddenly developed epilepsy, she began "hearing" voices with the same speech impediments as herself. "She initially heard her own voice speaking aloud, then the voices of hospital staff," says Daniela Hubl at the University Hospital of Psychiatry in Bern, Switzerland, a member of the team that treated her. "They had the same speech impediments as she did. It proves that the voices were generated in the language areas of the patient's own brain." The hallucinations disappeared when the woman received drugs to control her epilepsy (The Lancet, vol 370, p 538). Hubl believes the case is unique and supports more strongly than ever the scientific consensus that "voices" and other hallucinations experienced by people with conditions like schizophrenia are generated within their own brains. From issue 2617 of New Scientist magazine, 20 August 2007, page 16 © Copyright Reed Business Information Ltd.

Keyword: Language
Link ID: 10617 - Posted: 06.24.2010

US scientists may have discovered why long nerve cells do not break when you move or stretch your limbs. Experiments in worms showed that when a protein called beta spectrin is missing, nerve cells are brittle and break, leading to paralysis. The finding may help to explain why people with a condition called spinocerebellar ataxia progressively lose co-ordination and movement. The University of Utah study is in the Journal of Cell Biology. Humans have four genes responsible for the production of beta spectrin protein. Recent studies have shown that people with a condition called spinocerebellar ataxia type 5, a neurodegenerative disease that develops between the ages of 10 and 68, have a mutation in one of the genes. It was previously thought that the mutation in this protein meant cells could not communicate properly because the necessary proteins would not be anchored in place. But research by Professor Michael Bastiani and colleagues at the University of Utah suggests that a mutation in or absence of the protein causes long nerve fibres (axons) to lose their flexibility and break. When nematode worms were bred without beta spectrin their nerve axons died over time and caused paralysis. In worm embryos only 3% of nerve cells were broken or defective but that grew to 60% by the time the worms were a day old, suggesting the protein is not responsible for initial growth of nerve cells but for preventing breakage later on. Professor Bastiani said the team found it "incredible" that the one protein was responsible for preventing nerves breaking in your whole body. "The entire functioning of the nervous system depends on these wire-like axons between nerve cells," he said. (C)BBC

Keyword: Development of the Brain
Link ID: 10616 - Posted: 08.18.2007

By David Biello Sugar and spice and everything nice hold no interest for a cat. Our feline friends are only interested in one thing: meat (except for saving up the energy to catch it by napping, or a round of restorative petting) This is not just because inside every domestic tabby lurks a killer just waiting to catch a bird or torture a mouse, it is also because cats lack the ability to taste sweetness, unlike every other mammal examined to date. The tongues of most mammals hold taste receptors—proteins on the cellular surface that bind to an incoming substance, activating the cell's internal workings that lead to a signal being sent to the brain. Humans enjoy five kinds of taste buds (possibly six): sour, bitter, salty, umami (or meatiness) and sweet (as well as possibly fat). The sweet receptor is actually made up of two coupled proteins generated by two separate genes: known as Tas1r2 and Tas1r3. When working properly, the two genes form the coupled protein and when something sweet enters the mouth the news is rushed to the brain, primarily because sweetness is a sign of rich carbohydrates—an important food source for plant-eaters and the nondiscriminating, like humans. But cats are from the noble lineage Carnivora and, unlike some of its lesser members, such as omnivorous bears or, even more appalling, herbivorous pandas, they exclusively eat meat. © 1996-2007 Scientific American, Inc.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 10615 - Posted: 06.24.2010

Any homeowner knows that squirrels are clever – they hide nuts and food underground and return later in the year to dig up the lawn and eat; they never seem at a loss to find a way into your house and live between the walls rather than up in a tree. But squirrels are also clever when it comes to defending against predators. Adult squirrels have the ability to neutralize rattlesnake venom; and they also widely employ the tactic of "tail flagging" – pointing their tails straight up like a sword and waving them from side to side – to scare snakes off. But young squirrels are not immune to rattlers' venom. Luckily their parents have a lightsaber-like trick to defend them. Biologists using infrared cameras at University of California Davis .html discovered that since rattlesnakes can sense infrared radiation, the adult squirrels heat up their tails. Graduate student Aaron Rundus and his colleagues at UC Davis exposed California ground squirrels to rattlesnakes in the lab. When they viewed the interaction through an infrared video camera, they saw that the squirrels' tails heated up like a red-hot poker. But if they put a gopher snake, which cannot sense infrared radiation, in with the squirrels, the squirrels' tails remained dark and cold while they waved them. But questions still remained. © ScienCentral, 2000-2007

Keyword: Vision
Link ID: 10614 - Posted: 06.24.2010

Nathan Seppa An experimental vaccine for people who have multiple sclerosis has proved safe, clearing a necessary first hurdle toward regulatory approval. The results of this initial trial also suggest that the vaccine can indeed quell the self-destructive immune reaction that many scientists believe causes the disease. Despite this early promise, the researchers caution that the findings are based on data gathered from a small group over a limited time. The researchers used a technique called DNA vaccination, which introduces a gene into the body to elicit an immune response. But rather than rile the immune system against a foreign foe, the new multiple sclerosis (MS) vaccine seeks to induce immune tolerance of myelin basic protein, a component of myelin. A fatty material that protects nerves, myelin is degraded in MS, robbing patients of muscle control. For the vaccine, researchers at Stanford University and Bayhill Therapeutics in Palo Alto, Calif., designed a DNA ring that encodes a slightly altered version of myelin basic protein. The changes replaced immune-stimulating parts of the protein with immune-suppressing ones. Scientists gave 30 MS patients four injections over 9 weeks and then tracked their progress for a year. The study was made public this week and will appear in the October Archives of Neurology. ©2007 Science Service

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 10613 - Posted: 06.24.2010

By Greg Miller In hot deserts, animals must get water any way they can. A new study sheds light on what has to be one of nature's most bizarre adaptations to dry environments: Certain lizards have a network of tiny channels in the spaces between their scales that can suck up water from the ground (or from rain falling on their back) and transport it to their mouth for drinking. Researchers have suspected for decades that some desert lizards can harvest rainwater through their skin. The Australian thorny devil (Moloch horridus), for example, rubs its belly into the wet sand after a rain. In the 1920s, inquisitive researchers put this lizard in a shallow bowl of water and noticed that its entire body soon looked wet. "The initial thought was that they just took the water in directly through their skin," says Wade Sherbrooke, a biologist at the American Museum of Natural History's Southwestern Research Station in Portal, Arizona. But that turned out to be wrong. Unlike amphibian skin, which lets water through, reptile skin keeps precious water inside the body, Sherbrooke says. So how were the lizards transporting water? Later research suggested that water somehow traveled along the "scale hinges" in between the lizards' scales. In the new study, Sherbrooke and colleagues at James Cook University in Townsville, Australia, used light and electron microscopes to examine the scale hinges in detail. They discovered that the hinges contain tubelike channels about the width of one or two human hairs, a good size for harnessing capillary forces to draw in water. © 2007 American Association for the Advancement of Science.

Keyword: Miscellaneous
Link ID: 10612 - Posted: 06.24.2010

Katharine Sanderson Mice can smell carbon dioxide at levels just higher than that in normal air, thanks to specialized neurons in their nose. Minmin Luo at the National Institute of Biological Sciences, Beijing, and his colleagues tracked down the neurons that mice use to detect carbon dioxide, they write in Science1. The level of CO2 above which the mice smelled the gas, they report, was just 0.066% — about twice the average level of CO2 in the atmosphere (0.038%), but much less than the concentration in exhaled breath (about 4.5%) or the level considered safe for humans (0.5%). The team targeted neurons in the mouse nose that were already known to express the CO2-processing enzyme carbonic anhydrase type II (CAII). These cells, called guanylyl cyclase D cells, glowed in the presence of CO2, showing when mice were picking up the scent. Carbon dioxide can't be smelled by humans, but other animals have shown an ability to detect relatively high levels of the gas. Insects, too, can detect CO2, but they do it via membrane receptors rather than through any kind of nose. Luo's research shows that, to his surprise, in mammals this isn't the case — the mice are literally smelling the gas. "We did not expect it at all," he says. "Most people don't think CO2 is an odorant. It is used as an irritant, not an olfactory cue." ©2007 Nature Publishing Group

Keyword: Chemical Senses (Smell & Taste)
Link ID: 10611 - Posted: 06.24.2010

Rafael Caruso If we go from the outdoors on a bright sunny day into a very dimly lit room, we are hardly able to see our surroundings at first. As time goes by, however, we gradually become able to detect the room's contents. This phenomenon is known as "dark adaptation," and it typically takes between 20 and 30 minutes to reach its maximum, depending on the intensity of light exposure in the previous surroundings. The human retina can perform its light-detection function in an astounding range of light intensities, from bright sunlight to dim starlight, by relying on two types of light-sensitive cells, or photoreceptors. The first, the cones, evolved for day vision and can respond to changes in brightness even in extremely high levels of illumination. (Cones are unable to respond to light reliably in dim illumination, however.) Photoreceptors for night vision are called rods. Rods can act as light detectors even in extremely low levels of illumination but are ineffective—they are known to "saturate"—in bright light. Remarkably, rods can respond reliably to a single visible light photon, so they operate at the physical limit of light detection. Both cones and rods participate in dark adaptation, slowly increasing their sensitivity to light in a dim environment. Cones adapt faster, so the first few minutes of adaptation reflect cone-mediated vision. Rods work slower, but since they can perform at much lower levels of illumination, they take over after the initial cone-mediated adaptation period. This is actually a general feature of many sensory systems: if a sensation relies on stimulation of more than one type of receptor cell, the most sensitive receptor type at any given time is the one that mediates sensation. © 1996-2007 Scientific American, Inc.

Keyword: Vision
Link ID: 10610 - Posted: 06.24.2010

Heavy cheeses like stilton are the worst culprits for nightmare inducing sleep The best-known is that of the chemist Kekulé, who was puzzled by how the carbon atoms of benzene fitted together until he dreamt of snakes biting head to tail in a ring. However, that scarcely counts, for it was a daydream on a Clapham omnibus (he was looking blankly out of the window, as chemists often do). The science of dreams is, in many ways, a nightmare, plagued by untestable ideas conjured up by those with more inventiveness than insight. I once tried Freud's The Interpretation of Dreams and could make nothing of it, although many unhappy people believe its claim that unconscious misery reflects conscious experiences that, when recovered, may offer a cure. We mostly dream during paradoxical sleep (once called REM sleep, after the rapid eye movements that happen as the brain becomes almost as active as when awake). REM is remarkable: a whole group of molecules involved in nerve transmission is shut down and the body becomes almost paralysed (which is why when you dream of running you do not kick your partner to death). Perhaps a paradoxical snooze gives the receptors for those nerve transmitters a chance to restore themselves before the challenges of the morning. © Copyright of Telegraph Media Group Limited 2007

Keyword: Sleep
Link ID: 10609 - Posted: 06.24.2010

By Michael Balter Every parent can use a little help now and then, and birds are no exception. Some species even use nannies to feed and care for chicks. These "daycare" babies don't seem to do any better than offspring raised by mom and dad alone do, however, and researchers have struggled to figure out how birds benefit from the assistance. A new study has cracked the mystery: The nannies apparently allow mother birds to save their strength so they can lay eggs later on. In most bird species, males and females pair up to rear the brood. But about 3% of bird species are cooperative breeders: Only one female in a group lays eggs, and the rest of the adults help feed the chicks. Although several studies have shown that chicks get more to eat when helpers are present, little evidence indicates that they grow faster or have a higher survival rate. These findings have led some researchers to propose that the system benefits the helpers rather than the chicks, perhaps because the helpers receive reciprocal aid if they become breeders later on. A team led by biologist Andrew Russell of the University of Sheffield, U.K., set out to evaluate the costs and benefits of cooperative breeding in the superb fairy-wren of southeastern Australia. This species can breed in pairs and in groups of about 6 to 12 birds, which allows a comparison between the two strategies. In a study population made up of 68 bird nests, the researchers found that chicks that were raised in groups received 19% more food than those fed by their parents alone. Yet those chicks were no larger. The secret, the team reports in the 17 August issue of Science, was that eggs laid by females in cooperative groups were 5% smaller than those laid by females who bred in pairs, and their yolks had 12% less lipids and 13% less protein. Thus, the chicks started out smaller but caught up because they were fed more. © 2007 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Evolution
Link ID: 10608 - Posted: 06.24.2010

Ewen Callaway A study showing how HIV could prevent the brain from making new neurons offers an explanation for why some AIDS patients get dementia — and suggests a possible treatment. Dementia due to HIV is the leading cause of cognitive decline in people under 40 years of age, says Stuart Lipton, a biologist at the Burnham Institute for Medical Research in La Jolla, California, who led the study in Cell Stem Cell1. Researchers aren't sure what causes the condition, which afflicts 10-30% of people with HIV and causes symptoms including forgetfulness and leg weakness. If untreated with antiretroviral drugs, sufferers can turn comatose. Biologists have two theories to explain AIDS-related dementia. It could be that when HIV infects a type of white blood cell called a macrophage, the cell pumps out inflammatory chemicals to battle the infection that also, unfortunately, wipe out neurons. Or HIV could inflict its damage more directly. One previous study showed that a protein in the virus's shell — called gp120 — can stop brain stem cells from dividing2. Such new stem cells are needed to make new neurons. To investigate, Lipton and postdoc Shu-ichi Okamoto studied a strain of mice genetically engineered to make the virus's gp120 protein. Under the microscope, the mouse brains look just like those of humans with AIDS-related dementia, says Lipton. ©2007 Nature Publishing Group

Keyword: Neuroimmunology; Neurogenesis
Link ID: 10607 - Posted: 06.24.2010

Nora Schultz New Caledonian crows, famed for their tool-making skills, can also use tools to manipulate other tools. Such “metatool” use shows that the crows have the brainpower to apply their skills to a completely new situation and plan ahead to solve a task, researchers believe. Working with captured wild crows, Russell Gray and his team from the University of Auckland in New Zealand hid a treat in a box so that a crow could only extract it with the help of a long stick. This kind of task is easy for the tool-using crows. But then the researchers added a twist by placing the long stick in a cage, out of the crows' reach. No problem: the birds used a second, shorter stick, to get the first one, then took it back to the box to get the food. “Six out of seven crows tried straight away to use the short stick to get to the long tool. There was no trial and error,” says Gray. Metatool use is normally only seen in humans and apes. Even monkeys struggle in similar experiments. This is thought to be due to the cognitive complexity of the task, which requires using a tool on an intermediate object in a novel context before tackling the real goal, which is to extract the food. © Copyright Reed Business Information Ltd.

Keyword: Intelligence; Evolution
Link ID: 10606 - Posted: 06.24.2010

Matt Kaplan Some snakes are known to be able to go without food for periods of nearly two years. Until recently, the mechanism behind this unique skill was unknown, but new research has revealed some previously-unknown serpentine tricks. These may form the key adaptation that has kept this highly specialized group alive since before the days of Tyrannosaurus rex, biologists say. Biologists have long argued that there are two main tactics used by animals to weather a period of starvation. The core body temperature can be reduced, as is the case in penguins that go through torpor to reduce their calorie use during the winter. Hibernating animals such as hedgehogs utilize another method by stocking up on food and then reducing activity levels. Some species, including polar bears, do both. Snakes, it would seem, have an altogether different strategy at their disposal — they can save on energy use without lowering their temperature and while staying fully alert. As a bonus, they can also go hungry for longer without starting to 'eat' their own body from the inside. Biologist Marshall McCue at the University of Arkansas, Fayetteville, kept ratsnakes, pythons, and rattlesnakes in cages where they could not alter their activity levels — they were forced to be inactive. They were also unable to reduce body temperature, stuck with the laboratory temperature of a steady 27 ºC. The animals were then starved for a period of up to 168 days. ©2007 Nature Publishing Group

Keyword: Obesity
Link ID: 10605 - Posted: 06.24.2010

Ewen Callaway Scientists have erased a long-term memory in the brains of laboratory rats, offering insight into how such memories are stored. Yadin Dudai and Reut Shema of the Weizmann Institute of Science in Rehovot, Israel, trained rodents to associate a particular smell with illness. Injecting the rat brains up to a month later with a polypeptide called ZIP caused the rats to completely forget the unpleasant memory, they report in Science1. The study suggests that even though long-term memories can last for years or even for a lifetime, they are constantly maintained by an ever-active process. That goes against previous ideas that long-term memories are simply held in safe, static storage says co-author Todd Sacktor, a neuroscientist at State University of New York Downstate Medical Center in Brooklyn. "The result is surprising because most people would basically say it's impossible to erase a memory like this," says Sacktor. Most neuroscientists think that relatively permanent changes in the shape and physiology of neurons help store long-term memories, he says. Researchers already knew that if they caught the formation of a memory within minutes, they could wipe it from the brain's hippocampus with chemicals that stop neurons from making new proteins. ©2007 Nature Publishing Group

Keyword: Learning & Memory
Link ID: 10604 - Posted: 06.24.2010

A vaccine designed to tackle multiple sclerois has passed initial safety tests, say Canadian scientists. It is hoped that the BHT-3009 jab might reduce the damaging immune system attacks which cause the disease. Early checks were carried out on 30 patients at Montreal Neurological Institute, reported the journal Archives of Neurology. A British expert said that the way was clear for bigger trials - perhaps showing real benefits to patients. There is no cure for MS, which happens when the body's own defence system launches an attack on the tissue that surrounds nerve fibres, causing irreversible and worsening symptoms such as weakness and vision loss. DNA vaccines are already used in healthy patients to protect against infectious diseases, but the latest idea is to give them to patients with an existing disease such as MS. The Montreal researchers said they thought their study was the first time that a DNA vaccine had been given to someone with an "auto-immune" disease. Animal experiments have suggested that it might be possible to tweak the body's immune system so that the unwanted self-harming response becomes smaller, slowing the progress of the disease. The small-scale Montreal trial - using 30 MS patients - was designed to check that the vaccine would not cause any unexpected side-effects in advance of large-scale trials. The scientists also checked to see if there was any evidence in the tiny number of patients who received the vaccine that it was having an effect on their disease. (C)BBC

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 10603 - Posted: 08.15.2007

By CARL ZIMMER To understand the rules that govern life, biologists often seek out the weird extremes. And when it comes to family life, it is hard to find a weirder example than that of a common wasp known as Copidosoma floridanum. “You couldn’t dream up a more surreal life cycle than these guys have,” said Mike Strand, a professor at the University of Georgia. Copidosoma floridanum, native throughout the United States, is a parasite. The female wasps lay one or two eggs inside the egg of the cabbage looper moth. As the host egg develops into a caterpillar, the wasp egg grows into a microscopic cluster of grapes. Each grapelike mass of cells develops into a wasp embryo. A single egg can give rise to more than 3,000 genetically identical siblings, each about a fifth of an inch long. “The caterpillar is about two to three inches long, so you can stuff a lot of wasps in there,” Dr. Strand said. Most of the larvae are maggotlike creatures that drink the caterpillar’s blood. But up to a quarter of the wasps take on an entirely different form. They develop slender, snakelike bodies and rasping jaws. Instead of slurping blood, these hundreds of soldiers attack other wasp larvae. “They just latch on and suck away,” Dr. Strand said. The blood-suckers that are not killed by the soldiers eventually begin to devour the organs of their host, become pupae, and then develop into adults that fly away. The soldiers, on the other hand, cannot escape. “It’s lights out for the soldiers when their siblings eat the caterpillar,” Dr. Strand said. Copyright 2007 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 10602 - Posted: 06.24.2010