Oct. 26, 1997 News Tips -- University Of Maryland Research, 27th Annual Meeting, Society For Neuroscience
HERBAL BRAIN-CELL ARMOR -- Two compounds isolated from a type of ginseng may be potent neuroprotectors, researchers from the University of Maryland School of Medicine and the Seoul National University have found.
Tae H. Oh, PhD, professor of anatomy and neurobiology at Maryland, and Young C. Kim, Ph.D., from Seoul National University in Korea, studied the effects of ginsenosides Rb1 and Rg3 on cortical cells from rats. The compounds effectively inhibited overproduction of cell-killing nitrous oxide, which routinely follows nerve-cell poisoning by a naturally occurring amino acid byproduct called L-glutamate. They also inhibited formation of a dangerous compound called malondialdehyde and raised diminished levels of helpful superoxide dismutase in glutamate-treated cells.
Oh, a researcher at the medical school in Baltimore, and Kim, a Korean colleague, will present a poster on their findings on Wednesday, October 29, 1997, at the Society for Neuroscience annual meeting in New Orleans.
PAIN IS A TWO-WAY STREET -- Pain messages are transmitted up the nerves from pain receptors through the spinal cord to the brain, following routes known as ascending neural pathways. Another important kind of message—pain modulation, which affects how we react to pain—is transmitted downwards from the brain, along descending neural pathways.
Now Ronald Dubner, DDS, PhD, and colleagues Ke Ren, MD, PhD, and Fong Wei, PhD, at the Dental School, University of Maryland, have determined that after inflammation and injury, the descending neural pathways in the spinal cord contain both kinds of neurons: ones that enhance pain messages and others that inhibit them. When they destroyed neurons that originate in one region of the rats’ brainstem, called the nucleus raphe magnus, the rats experienced more pain. But when neurons from the nearby nucleus gigantocellularis were destroyed, the animals experienced less pain.
Dubner is chairman of the Department of Oral and Craniofacial Biological Sciences. Ren, an assistant professor, and Wei, a postdoctoral fellow in the same department, will report their findings on Wednesday, October 29, 1997 at the Society for Neuroscience annual meeting in New Orleans.
WHERE (EXACTLY) DOES IT HURT? -- No matter whether you smash your thumb with a hammer, splatter hot cooking oil in your face or slash your foot on a sliver of broken glass, your perception of pain arises from activity in your brain. New research being conducted by neuroscientists at the Dental School, University of Maryland, is closing in on the regions of the brain responsible for the perception of pain.
In a study analyzing the sensory capacities and extent of brain damage in six individuals with injuries involving two parts of the brain commonly believed to be pain processing regions, Joel D. Greenspan, PhD, assistant professor in the Department of Oral and Craniofacial Biological Sciences, and colleagues Roland R. Lee, MD, and Fred A. Lenz, MD, found that a central region of the cerebral cortex called the posterior parietal operculum plays a key role in our recognition of injurious stimuli as painful. Another region suspected to have some role in pain responses—the insular cortex—in fact can be damageed extensively without altering the threshold of pain, Greenspan said. Other studies suggest, however, that the insular cortex may play a role in people’s emotional responses to pain.
He will present a poster on their preliminary findings on Sunday, October 26, 1997 at the Society for Neuroscience annual meeting in New Orleans.
HELPLESS RATS HELP TEST DEPRESSION DRUG THERAPIES -- In an animal model of depression developed by researchers at the University of Maryland School of Pharmacy, cytochrome oxidase - an enzyme that limits the rate of mitochondrial oxidative metabolism - can be used to map synaptic activity and to study specific responses to new drug therapies at a cellular and local level in the brain.
Emmeline Edwards, PhD, associate professor, and colleagues in the school’s Department of Pharmaceutical Sciences, found baseline differences in brain metabolic capacity using a learned-helplessness rat model of depression. The researchers’ model was systematically bred to foster increased susceptibility to learned helplessness and is in its 40th generation. Cytochrome oxidase histochemistry in this study indicated a decreased capacity for oxidative energy metabolism in the cingulate cortex, a limbic system structure implicated in depression, Edwards will report on Tuesday, October 28, 1997 at the Society for Neuroscience Annual Meeting in New Orleans.
Edwards also will report on findings that the depression model can be used to study specific opioid mechanisms in depression. She hopes this will enable researchers to assess genetic susceptibility to depression linked with drug abuse. Future studies may lead to alternative strategies for treating those with both depression and addiction.
The Maryland researchers are presenting two additional posters highlighting other applications of their depression model.
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