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| Name: |
Raymond J. Dingledine |
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| Position: |
Professor and Chair of Pharmacology
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| Degree: |
Ph.D., Stanford University, 1975
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| Programs: |
MSP,
Full Member
NS,
Full Member
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| Phone: |
404 727-5982 |
| Address: |
5001 Rollins Research Center, 1510 Clifton Rd, 1940/001/1AF
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| Email: |
rdingledine@pharm.emory.edu |
| Website: |
http://www.pharm.emory.edu/dingledine-4.htm |
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Research Descriptions:
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Short:
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Genetic control of glutamate receptor function.
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Long:
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Why is the hippocampus so vulnerable to seizures and seizure-induced damage? Which changes in neuronal circuitry underlie the gradual transition from a normal brain to a brain with epilepsy? How is the normal function of glutamate receptors in synaptic transmission regulated at the transcriptional and translational levels? How does activation of glutamate receptors kill neurons in the brain? How can we take advantage of the large number of modulatory sites on glutamate receptors to develop new drugs and new therapeutic strategies for epilepsy and stroke-induced brain damage? These are some of the questions that drive research in our laboratory. Glutamate receptors mediate the vast majority of excitatory synaptic transmission in the brain. We combine electrophysiological and molecular biological techniques to identify the postsynaptic glutamate receptors in key pathways in the rat hippocampus, and to study the cellular and molecular basis for epilepsy in this brain region. Recombinant glutamate receptor subunits, and subunit mutants, are expressed in Xenopus oocytes and mammalian cell lines in order to identify and characterize the modulatory sites on receptors of known subunit composition. This combination of molecular studies of cloned glutamate receptors, and functional studies of neurons in hippocampal slices, should lead to a better understanding of the roles these membrane signalling proteins play in health and disease.
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