Grid1 expression in female rats at 7 days withdrawal from chronic intermittent ethanol exposure

Description

Substance use disorders and withdrawal processes are chronic health disorders that remain a large burden on individuals and continue to strain the health care system in numerous ways. Understanding how said disorders manifest and persist across the life span of individuals will aid in the development of treatment plans and therapeutic targets. It is known that during substance withdrawal, functional alterations occur that accentuate an individual’s risk for repeated use. The current study aims to understand if alterations in the structure of neuron communication sites play a role in the development/expression of functional increases, which in turn may contribute to withdrawal symptoms and thus a user’s predisposition to relapse. We are exploring the expression of Grid1, a delta-type glutamate receptor, which 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, female rats were exposed to ethanol vapor and then placed into a 7-day period of abstinence. Brains were then extracted and treated with sulfo-NHS-S-S-Biotin to label extracellular proteins. Utilizing western blot techniques and Grid1 antibodies, we compared the relative amount of protein expression in our samples, to control animals using student t-tests (p< 0.05 for significance).

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Grid1 expression in female rats at 7 days withdrawal from chronic intermittent ethanol exposure

Substance use disorders and withdrawal processes are chronic health disorders that remain a large burden on individuals and continue to strain the health care system in numerous ways. Understanding how said disorders manifest and persist across the life span of individuals will aid in the development of treatment plans and therapeutic targets. It is known that during substance withdrawal, functional alterations occur that accentuate an individual’s risk for repeated use. The current study aims to understand if alterations in the structure of neuron communication sites play a role in the development/expression of functional increases, which in turn may contribute to withdrawal symptoms and thus a user’s predisposition to relapse. We are exploring the expression of Grid1, a delta-type glutamate receptor, which 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, female rats were exposed to ethanol vapor and then placed into a 7-day period of abstinence. Brains were then extracted and treated with sulfo-NHS-S-S-Biotin to label extracellular proteins. Utilizing western blot techniques and Grid1 antibodies, we compared the relative amount of protein expression in our samples, to control animals using student t-tests (p< 0.05 for significance).