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Mice treated with the antidepressant Prozac early in life grow into adults with emotional problems, a new report concludes. Whether the drug has the same effect on people is unknown. But the result will add to the growing debate over what risks Prozac (fluoxetine) and similar SSRI drugs (selective serotonin reuptake inhibitors) pose for young children and unborn babies. "If they really need these drugs, people should take them. They can be life savers," says Jay Gingrich, a psychiatrist at Columbia University in New York City, US, who led the research. "But it is a little bit alarming to find they might carry risks that aren't apparent until later in life." Researchers began injecting mice with fluoxetine four days after birth until they were 21 days old. Nine weeks after their last injection, the adult animals were given a series of behavioural tests designed to assess their level of anxiety and depression. The team found that rodents who received drug as newborns were more intimidated by new surroundings and moved more slowly to avoid painful shocks compared to controls. "They are more inhibited in novel situations," says Gingrich. "Extrapolating to people, we'd say the mice are showing symptoms of anxiety and depression or emotional problems." © Copyright Reed Business Information Ltd.
Keyword: Depression; Development of the Brain
Link ID: 6325 - Posted: 06.24.2010
Jim Giles Connecting a battery across the front of the head can boost verbal skills, says a team from the US National Institutes of Health. A current of two thousandths of an ampere (a fraction of that needed to power a digital watch) applied for 20 minutes is enough to produce a significant improvement, according to data presented this week at the annual meeting of the Society for Neuroscience, held in San Diego. And apart from an itchy sensation around the scalp electrode, subjects in the trials reported no side-effects. Meenakshi Iyer of the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, ran the current through 103 initially nervous volunteers. "I had to explain it in detail to the first one or two subjects," she says. But once she had convinced them that the current was harmless, Iyer says, recruitment was not a problem. The volunteers were asked to name as many words as possible beginning with a particular letter. Given around 90 seconds, most people get around 20 words. But when Iyer administered the current, her volunteers were able to name around 20% more words than controls, who had the electrodes attached but no current delivered. A smaller current of one thousandth of an amp had no effect. ©2004 Nature Publishing Group
Keyword: Learning & Memory
Link ID: 6324 - Posted: 06.24.2010
Jim Giles When the star of the movie Super Size Me ate only McDonald's for a month, his physical health went down the tube. Now researchers have warned that such diets could hit mental abilities too. Although this idea has been suggested before, a slew of animal studies, unveiled on 25 October, all conclude that learning and memory suffer when fat intake rises. Rats and mice raised on the rodent equivalent of junk food struggle to learn their way around a maze and take longer to recall the solution to problems they have already solved, researchers said at the annual meeting of the Society for Neuroscience, held in San Diego. In one experiment, rats were asked to remember the position of platforms in a pool of water; the animals are motivated to do so because they dislike swimming. Two groups took the test: controls and a set that had munched on a high-fat and high-cholesterol diet for eight weeks. "Those on the high-fat diet made many more mistakes," says Ann-Charlotte Granholm of the Medical University of South Carolina in Charleston. Another study challenged mice to learn how to navigate a maze without running over areas that gave them mild electric shocks. When John Morley and colleagues at Saint Louis University in Missouri tested the mice a week after they had learned the task, those raised on a high-fat diet took significantly longer to remember how to avoid the shocks. ©2004 Nature Publishing Group
Keyword: Learning & Memory; Obesity
Link ID: 6323 - Posted: 06.24.2010
- US target discovery company Psychiatric Genomics has shed new light on the mechanisms behind schizophrenia, pointing to a possible new cellular target that does not rely on modulating the levels of neurotransmitters in the brain. The company’s results showed that the expression levels of genes encoding for energy metabolism and protein processing are selectively and consistently decreased in the brains of patients with schizophrenia. In the first study of its kind, scientists from Psychiatric Genomics microdissected neurons from the hippocampus of post-mortem brain samples of psychiatric patients and, using microarray technology, compared them to those same neurons from people not affected by the disease. The integrity of the findings was supported by their high statistical significance, their replication in two different groups of schizophrenia patients, and the lack of such changes in neurons either from non-afflicted subjects or from patients with bipolar disease or depression. © 2000/2004– NOVIS
Keyword: Schizophrenia
Link ID: 6322 - Posted: 06.24.2010
Human primitive spinal cord cells delayed symptoms and paralysis by a week when implanted in the spinal cord of rats destined to develop amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease, researchers from Johns Hopkins report. The human neuronal stem cells were obtained from embryos by scientists at biotech company Neurostem Inc., transferred to Hopkins and implanted into the lower part of the rats' spinal cords about a month before the animals usually develop muscle control problems characteristic of ALS. The treatment delayed the animals' death by 11 days. Research associate Leyan Xu, Ph.D., is scheduled to present the results Oct. 23 at the annual meeting of the Society for Neuroscience in San Diego. "This rat model of ALS progresses very rapidly -- within two or three weeks of symptoms appearing, the rats have to be euthanized -- so the delay we saw is quite significant," says the study's senior author, Vassilis Koliatsos, M.D., associate professor of pathology, neurology, neuroscience and psychiatry and behavioral sciences at Hopkins. "Our study is proof of principle, that neuronal stem cells do have potential in conditions caused by separation within the nervous system, whether by disease or injury."
Keyword: ALS-Lou Gehrig's Disease
Link ID: 6321 - Posted: 10.26.2004
By LINDA CARROLL Parents want their children to succeed. And these days, toy store shelves are filled with products with names like Baby Einstein and Brainy Baby. The toy manufacturers do not come out and say it, but the clear implication is that babies who play with these toys may score some extra I.Q. points and get an early start on the road to an Ivy League college. Attuned to the increasing awareness among parents that the first three years are critical developmentally, companies are increasingly positioning their products as vital to optimizing intellectual growth. Child development experts, however, have their doubts. No studies exist, they point out, to show that any of the toys or videos give children an intellectual edge over playmates who stick to old-fashioned building blocks and baby dolls. While researchers have found that some babies who are deprived of certain stimuli during the first years of life never completely recover, they have yet to demonstrate that increasing stimulation makes babies smarter. And some experts believe that the toys may even be detrimental to development because they lead children to focus on memorization rather than imagination and problem-solving abilities. Copyright 2004 The New York Times Company
Keyword: Development of the Brain; Intelligence
Link ID: 6320 - Posted: 10.26.2004
Cranking up female sex drive, it may have played an important role in early societies By Liz Brown Breastfeeding women and their babies may hold the secret to developing a drug that could increase female sex drive. American researchers at the University of Chicago in Illinois have found that women's sex drive increased up to 24% after being exposed to breastfeeding compounds for two months. "This is the first report in humans of a natural social chemosignal that increases sexual motivation," says Martha McClintock, lead researcher. Though not necessarily perceived as odors, chemosignals affect mood and menstrual cycles when absorbed through the nose. To conduct the study, the researchers recruited 26 breastfeeding women and asked them to wear pads in their nursing bras and underarms. The pads collected infant saliva, perspiration and sweat, and the scientists then cut them into pieces and froze them. Copyright © 2002-2004 Betterhumans
Keyword: Sexual Behavior; Chemical Senses (Smell & Taste)
Link ID: 6319 - Posted: 06.24.2010
Many children slink past bed times the way the craftiest of thieves slip by security—with careful preparation and flawless backup plans. But new research shows that sleep-deprived middle-schoolers experience significant decreases in self-esteem, increased instances of depression and significant dips in grades. Jean Rhodes, professor of psychology at the University of Massachusetts at Boston, studied sleep in nearly 2,500 Chicago school children, aged 11 to 14-years-old. She reported in the January/February issue of the journal Child Development that as various factors suck the sleep out of children, a host of negative side effects result. "The fewer hours of sleep that children got, the more depressed they were, the higher number of depressive symptoms [they had], and the lower their self-esteem and the lower their grades," Rhodes explains. Biologically, middle school marks a child’s second largest growth spurt, a leap that dwarfs even the elementary school years, Rhodes says. As children grow and learn to steer past the pitfalls of puberty, they also learn to shuffle schedules filled with more and more activities. "There’s an increased need for sleep, yet at the same time middle-schooler’s lives are really complicated," Rhodes says. "They’re IMing (instant messaging), there are earlier school start times, extra-curricular [activities]…and so we know that this is a period of an increased need for sleep that’s clashing with an increased need to be awake." © ScienCentral, 2000- 2004
Keyword: Sleep; Development of the Brain
Link ID: 6318 - Posted: 06.24.2010
University of Toronto researchers have shown that human retinal stem cells transplanted into the eyes of mice and chicks can successfully regenerate. The research, published in the Oct. 19 issue of The Proceedings of the National Academy of Sciences, documents the development of transplanted human retinal stem cells into light-sensing photoreceptor cells and retinal pigment epithelial (RPE) cells, the cells which bounce light and images back onto the retina. "We transplanted the cells early in the animals' development when all the nutrients and signals they needed for differentiation were still there," says lead author Brenda Coles, a U of T laboratory technician working under the supervision of Professor Derek van der Kooy in the Department of Medical Genetics and Microbiology. "When their eyes fully developed, the human cells survived, migrated into the sensory part of the eye and formed the correct cells." The research has implications for future treatment of degenerative eye diseases such as retinitis pigmentosa and macular degeneration but that's still a long way off, says Coles. She, van der Kooy and their colleagues are now exploring whether retinal stem cells from healthy mice continue to develop into photoreceptor cells and RPE cells when transplanted to mice with diseased eyes.
Keyword: Stem Cells; Vision
Link ID: 6317 - Posted: 10.26.2004
SAN DIEGO--Doctors who treat patients with posttraumatic stress disorder (PTSD) have long sought a therapy that would erase bad memories, or at least keep them in check. Preliminary research on rats and humans presented here 24 October at the meeting of the Society for Neuroscience suggests that a drug already in wide use for treating high blood pressure might have just that effect. The drug, propranolol, blocks certain receptors for the neurotransmitter norepinephrine and has already shown promise in small clinical trials for PTSD, apparently preventing the formation of traumatic memories. In those studies, emergency room patients given propranolol within a few hours after an accident had fewer symptoms of posttraumatic stress months later. That suggested that propranolol could act as a prophylactic. The new work hints that propranolol might also work on memories that have already formed. Jacek Dębiec, a neurobiologist at New York University, conditioned rats to fear a tone by pairing it with a mild shock. After training, the rats freeze up in anticipation when they hear the tone. The next day, Dębiec refreshed the rats' memory, exposing them again to the tone and shock. He then gave half of the animals an injection of propranolol. Two days later, untreated rats still remembered what the tone meant; upon hearing it, they froze about 70% of the time. But rats given propranolol froze only about half as often, indicating a weaker memory for the fearful association between sound and shock. Even when Dębiec waited 2 months before reactivating the memory and delivering propranolol, the drug had a similar effect, he reported at the meeting and in a paper published in the current issue of Neuroscience. Copyright © 2004 by the American Association for the Advancement of Science.
Keyword: Learning & Memory; Emotions
Link ID: 6316 - Posted: 06.24.2010
EUGENE, Ore. -- A trusted mental map of your surroundings turns out to be slightly misaligned, skewing your orientation. Your ability to control the direction in which you move is similarly compromised, although in a manner opposite the map's offset. Taken together, the errors cancel one another, and you end up exactly where you want to be. Contrary to the proverb, two wrongs do make a right. This exception is the rule when it comes to how our brain processes what our eyes see and where our body moves, according to a discovery by University of Oregon researchers Paul Dassonville and Jagdeep Kaur Bala that will appear in the November issue of the journal PLoS Biology. Their study, funded by the National Science Foundation, challenged a dominant theory of how the brain processes vision. The theory holds that information from the eyes separates into two distinct streams: one to simply represent where we see things in the environment, and another to guide the physical movements of our body within that environment. Both processes have been thought to depend largely on accessing distinct maps of the environment within the brain, representing objects from varying locations in our field of vision by systematically varying activity in corresponding regions of the brain.
Keyword: Vision
Link ID: 6315 - Posted: 10.26.2004
by Rita Suri, M.D., and Lori L. Altshuler, M.D. Lifetime prevalence rates of major depressive disorder (MDD) in women are estimated to be as high as 21% (Kessler et al., 1993; Weissman et al., 1993). The postpartum period in particular represents a time of increased vulnerability for women (Cox et al., 1993; O'Hara et al., 1990), though postpartum disorders are often under-recognized and undertreated. Pregnant women generally receive little education about the possibility of depression after delivery, and because symptoms of depression can overlap with common postpartum symptoms, they may go unrecognized. Women may also feel ashamed of having negative emotions at a time when they "should be joyful" and thus not seek professional help. The DSM-IV defines postpartum depression as a major depressive episode with an onset in the first four weeks following childbirth. Although epidemiologic studies vary in the time frame used to define the postpartum period, ranging from four weeks to six months after delivery, the period of increased risk seems to occur relatively close to delivery. A study by Cox et al. (1993) of 232 postpartum women found that rates of depression were threefold higher in the five weeks after giving birth, but comparable at six months postpartum, when compared to a similarly matched control group of women who had not had a baby within the last 12 months. Wisner et al. (2004a) found that in 51 nondepressed women with a history of postpartum depression, 21 women developed a recurrent postpartum episode when followed for the year after childbirth. Five (24%) of these women experienced depression in the first postpartum month. © 2004 Psychiatric Times. All rights reserved.
Keyword: Depression; Hormones & Behavior
Link ID: 6314 - Posted: 06.24.2010
by Leo Sher, M.D. Light therapy, in one form or another, has been used as a treatment for a number of conditions since ancient times. Nearly 2,000 years ago, Greco-Roman physicians were treating depression and lethargy with sunlight directed toward the eyes. During his Arctic expeditions in the 1890s, Frederick Cook, M.D., noticing the profound influences of light on the voyagers and Alaskan natives, described a syndrome characterized by depressed mood, fatigue, and loss of energy and sexual desire. In 1946, H. Marx reported the use of bright artificial light to treat four men who had become depressed during an Arctic winter. Contemporary light therapy involves daily scheduled exposure to bright artificial light (Lam et al., 1999b; Partonen, 2001; Rosenthal and Matthews, 1999). The term light therapy is used to differentiate light therapy for psychiatric disorders from phototherapy for other conditions, such as hyperbilirubinemia or psoriasis. Since the first study of light therapy in winter seasonal affective disorder (SAD) (Rosenthal et al., 1984), a syndrome in which depression developed during fall or winter and remitted the following spring or summer for at least two successive years, numerous studies have concluded that bright light therapy is an effective treatment for SAD (Lam et al., 1999b; Magnusson and Boivin, 2003; Oren and Rosenthal, 1992; Partonen, 2001). © 2004 Psychiatric Times. All rights reserved.
Keyword: Depression; Biological Rhythms
Link ID: 6313 - Posted: 06.24.2010
by Richard C. Shelton, M.D. Currently available antidepressant medications are effective for a large segment of the population with depression. However, recent data suggest that a sizable portion of patients with unipolar depression do not experience full therapeutic recovery. For example, Simon et al. (1999) found that only about half of depressed patients treated with antidepressants in a primary care setting achieve recovery over a two-year period. Since lack of full response is common, management strategies need to be established and implemented. Current approaches include: the use of combination antidepressant treatments (e.g., selective serotonin reuptake inhibitor and bupropion [Wellbutrin]), augmentation (e.g., the addition of lithium [Eskalith, Lithobid] or thyroid hormone to an antidepressant), the addition of psychotherapy or electroconvulsive therapy (Shelton, 2003, 1999). However, even with these approaches, a significant minority of patients do not experience a full therapeutic effect. Recently, novel antipsychotics have shown some promise for the management of depressive disorders. From a mechanistic standpoint, the pharmacological properties of at least some of these drugs predict antidepressant properties. Novel antipsychotics act, to varying degrees, on a variety of dopamine, serotonin (5HT), glutamate and other receptors. The antagonism of 5HT2A receptors is common among these drugs, and blockade of this subtype is seen with other antidepressant agents such as mirtazapine (Remeron) and nefazodone (Serzone). Blocking of 5HT2C receptors has also been shown to enhance release of frontal dopamine and norepinephrine, which is thought to be a key antidepressant property (Shelton, 2003; Zhang et al., 2000). © 2004 Psychiatric Times. All rights reserved.
Keyword: Depression
Link ID: 6312 - Posted: 06.24.2010
SAN DIEGO – Students, keep this in mind before that next major exam: Pre-test jitters make it easier to recall memorized facts, but that stress also makes it tough to solve more complex problems. Researchers at Ohio State University gave a battery of simple cognitive tests to 19 first-year medical students one to two days before a regular classroom exam – a period when they would be highly stressed. Students were also given a similar battery of tests a week after the exam, when things were less hectic. While pre-exam stress helped students accurately recall a list of memorized numbers, they did less well on the tests that required them to consider many possibilities in order to come up with a reasonable answer. A week after the exam, the opposite was true. "Other studies have suggested that elevated stress levels can actually improve some aspects of cognition, particularly working memory," said Jessa Alexander, a study co-author and a research assistant in neurology at Ohio State. "The results of the two problem-solving tests we administered suggested a decline in problem solving abilities that required flexible thinking."
Keyword: Learning & Memory; Stress
Link ID: 6311 - Posted: 06.24.2010
Using an animal model system, researchers have advanced our understanding of Fragile X Syndrome by successfully visualizing individual mutant neurons in an otherwise normal brain. They find that brain neurons that fail to express appropriate levels of Fragile X protein are structurally abnormal and make defective connections to other neurons. The work is reported by a team led by Kendal Broadie at Vanderbilt University. Fragile X Syndrome is the most common type of inherited mental retardation. Since the early 1990's, it has been known that the disease results from the loss of a single gene and, for the last several years, that the Fragile X gene product regulates the expression of other proteins. However, the link between this molecular function and the Fragile X brain defect has remained a mystery. Employing a fruit fly model of the disease, the researchers utilized a new technique that allows the generation of single mutant nerve cells that are marked by their expression of a glowing fluorescent protein, making these nerve cells distinctly visible in an otherwise normal brain. In their experiments, the researchers were able to observe mutant nerve cells that either completely lacked the Fragile X protein or overexpressed it, the fluorescent protein label allowing the entire architecture of these neurons to be visualized in the intact brain.
Keyword: Genes & Behavior
Link ID: 6310 - Posted: 10.26.2004
The world’s first brain prosthesis has passed the first stages of live testing. The microchip, designed to model a part of the brain called the hippocampus, has been used successfully to replace a neural circuit in slices of rat brain tissue kept alive in a dish. The prosthesis will soon be ready for testing in animals. The device could ultimately be used to replace damaged brain tissue which may have been destroyed in an accident, during a stroke, or by neurodegenerative conditions such as Alzheimer’s disease. It is the first attempt to replace central brain regions dealing with cognitive functions such as learning or speech. To achieve their result, Theodore Berger and his colleagues at the University of Southern California in Los Angeles, US, had to develop a system that would “read” real neural signals from healthy tissue, process them just as the lost brain tissue should, and pass on the resulting signals to the next brain area. The brain region they are trying to replace is the hippocampus, which is vital for forming memories. The hippocampus has a well-understood three-part circuit. It also has a regular repeating structure, so elements of all three parts of the hippocampal circuit can be kept in a fully functional state, even in small slices in a culture dish. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 6309 - Posted: 06.24.2010
SAN DIEGO – Researchers at the OHSU Oregon National Primate Research Center (ONPRC) have identified a key gene that impacts the timing of puberty and can shorten the time span for reproduction. The research was led by Sergio Ojeda, Ph.D., head of the Division of Neuroscience and a senior scientist at ONPRC. The work will be presented at the Society for Neuroscience annual meeting on Oct 24, 2004 by Claudio Mastronardi, the lead author of the report. "Using a mouse model, our lab has determined that the absence in the brain's hypothalamus of a gene called TTF-1 causes a delay in the onset of female puberty," explained Ojeda. "This work is of particular interest to those investigating both the delay and early onset of puberty in young women. While there is no definitive information, recently a number of research papers have been published suggesting that young women are reaching puberty at an earlier age. Other research has suggested that if this is the case, it may be linked to the nation's obesity crisis." Prior to the research to be reported at the Society for Neuroscience meeting, Ojeda's group performed studies with rats showing that the TTF-1 gene is expressed in a discrete cellular subset of the hypothalamus during sexual development. Then, using a genome-wide approach, they determined that expression of the TTF-1 gene increases in the hypothalamus of nonhuman primates at the onset of puberty.
Keyword: Hormones & Behavior; Obesity
Link ID: 6308 - Posted: 06.24.2010
Regular exercise could halt Parkinson's disease, US researchers believe. In a study on rats, exercise prevented degeneration of nerve cells that are normally destroyed by the disease. The University of Pittsburgh researchers are now recruiting patients to see if regular exercise has the same effect in humans. They told a meeting of the Society of Neuroscience how exercise might stimulate key proteins vital for nerve cell survival. In Parkinson's disease, cells in the brain that contain a messenger called dopamine progressively die out. This means messages don't get through in the normal way, which causes the tell-tale signs of the disease such as uncontrollable tremors, slow movements and rigid limbs. There is some disagreement within the Parkinson's research community as to the benefits of intense exercise for people with PD. While none have reported harm caused by physical activity, some studies have shown no statistical positive influence of exercise. Dr Michael Zigmond and colleagues examined the brains of rats that had exercised for seven days before receiving a toxin that is known to induce a disease resembling Parkinson's in rodents. They compared these animals to rats that had not been exercised before receiving the toxin. Exercise appeared to protect the brain against Parkinson's-type damage. Fewer dopamine-containing nerve cells, or neurons, died in the exercised rats compared to the sedentary rats. The researchers believe exercise stimulates the production of proteins that are important for the survival of neurons. (C)BBC
Keyword: Parkinsons
Link ID: 6307 - Posted: 10.25.2004
By MARC SANTORA The disease's fatal grip on the brain seems to come out of nowhere, afflicting an otherwise healthy person and turning him into an incoherent muddle. In Ulster County in upstate New York, that was how death came to at least two people in the last year. The rare brain malady called Creutzfeldt-Jakob disease caused the death of one resident in November 2003 and of a second this fall. About one in a million people worldwide die from the mysterious disease each year, and there is no medical explanation for why the disease afflicts humans in its most common form. There has been a recent buzz in Ulster County about the strange illness, but only within the small circles of the victims' families. Then the community discovered that a 60-year-old woman had died in August from an illness that seemed similar to Creutzfeldt-Jakob disease. The woman's family did not allow an autopsy, so it cannot be determined if she had the disease. But after comparing notes, people found out that another person in nearby Dutchess County died of the disease this year. There have been other unusual deaths, including that of another woman in Ulster County, Colleen Staccio, 46, who died in August from a condition her doctors initially said was Creutzfeldt-Jakob disease but whose autopsy showed otherwise, and that of Richard Tobey, 59, who died of the disease two weeks ago. Copyright 2004 The New York Times Company
Keyword: Prions
Link ID: 6306 - Posted: 10.25.2004


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