Medications for Alcohol Withdrawal/Brain Damage
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505 Chicago Avenue, Evanston, IL, 60202
AbstractChronic ethanol ingestion results in neurodegeneration with loss of neurons, glial proliferation anventricular and subarachnoid space. Work from our laboratories has demonstrated that chronic ethanolanimals produces an up-regulation of the excitatory N-methyl-D-aspartate (NMDA) subtype of glutamateWe have recently implicated the NMDA receptor system in induction of excitotoxic damage to various nduring ethanol withdrawal. We will test a series of compounds for their effectiveness in protectingcerebellum and cerebral cortex, grown in culture, against ethanol withdrawal induced excitotoxic damthe effectiveness of a novel NMDA receptor channel blocker, (+)-5- aminocarbonyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine(ADCI), which we have previously shown to be an excellent agent fobehavioral hyperexcitability (tremor, convulsions) during ethanol withdrawal in animals. We will alscycloleucine, and low efficacy partial agonists i.e.,; 1-neuroprotective actions in our cell culturewithdrawal excitotoxicity. Finally, we will test a series of gangliosides, including GM1 and GT1b, shave been touted to protect against glutamate-induced excitotoxicity without compromising the initiarelated events accompanying NMDA receptor stimulation. Our studies will generate an understanding ofcompounds are most effective for preventing ethanol withdrawal excitotoxicity and provide a basis foanimals in Phase II of the SBIR program.
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