Grid1 expression in male rats at 14 days withdrawal from chronic intermittent ethanol exposure

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Substance use disorders are chronic health conditions that contribute a large burden on individuals and the healthcare system. Understanding how these use disorders develop and are maintained across the lifespan of individuals will aid in the development of treatment plans and possible therapeutics. It is known that during withdrawal from drug use, functional alterations occur that predispose/accentuate an individual’s risk to return to drug use. The current study seeks to identify if any alterations in the structure of neuronal communication sites plays a role in the development or expression of functional increases. As such, we are exploring the expression of Grid1, a delta type glutamate receptor, that plays a role in the formation of synaptic contacts between neurons. We hypothesize that Grid1 is dynamically regulated in response to withdrawal state dependent alterations in glutamate receptor function. To conduct these studies, male rats were exposed to ethanol vapor and then placed into forced abstinence for 14 days. Brains were extracted and treated with Biotin (sulfo-NHS-S-S-Biotin, Pierce, Cat. # 21331) to label extracellular proteins. Using western blot techniques and Grid1 antibodies we measured the relative amount of protein expression in our samples, in comparison to control animals using students t-tests (p< 0.05 for significance). Preliminary data are being analyzed. These data will be combined across a range of withdrawal times to gain a clearer understanding of how Grid1 expression is regulated during ethanol withdrawal.

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Grid1 expression in male rats at 14 days withdrawal from chronic intermittent ethanol exposure

Substance use disorders are chronic health conditions that contribute a large burden on individuals and the healthcare system. Understanding how these use disorders develop and are maintained across the lifespan of individuals will aid in the development of treatment plans and possible therapeutics. It is known that during withdrawal from drug use, functional alterations occur that predispose/accentuate an individual’s risk to return to drug use. The current study seeks to identify if any alterations in the structure of neuronal communication sites plays a role in the development or expression of functional increases. As such, we are exploring the expression of Grid1, a delta type glutamate receptor, that plays a role in the formation of synaptic contacts between neurons. We hypothesize that Grid1 is dynamically regulated in response to withdrawal state dependent alterations in glutamate receptor function. To conduct these studies, male rats were exposed to ethanol vapor and then placed into forced abstinence for 14 days. Brains were extracted and treated with Biotin (sulfo-NHS-S-S-Biotin, Pierce, Cat. # 21331) to label extracellular proteins. Using western blot techniques and Grid1 antibodies we measured the relative amount of protein expression in our samples, in comparison to control animals using students t-tests (p< 0.05 for significance). Preliminary data are being analyzed. These data will be combined across a range of withdrawal times to gain a clearer understanding of how Grid1 expression is regulated during ethanol withdrawal.