Document Type

Honors Thesis

Publication Date

Spring 5-2017

Abstract

Alcohol abuse is the fourth leading cause of preventable death in the United States (National Institute on Alcohol Abuse and Alcoholism [NIAAA], 2016). Alcohol affects us on a molecular, biological, and even societal level. Liver damage, cancer, and drunk driving accidents are only a few adverse consequences of alcohol abuse. Studies have also shown that alcohol abuse can damage the brain, in part by activating the central nervous system’s immune system, leading to inflammation and demyelination. This damage may lead to alcohol-related psychiatric disorders, motor impairment, and cognitive disabilities. Studies have also shown that females tend to exhibit more damage with less alcohol consumption than males, and that genetic background influences sensitivity to the drug. Thus, studying alcohol addiction at a biological level with special care for how sex and genetic background influence this phenomenon is key to understanding addiction and delivering effective treatment. In the present experiment, I examined the brain’s immune response to alcohol withdrawal by performing immunohistochemical analysis of microglial activation at two post-withdrawal time points in female C3H/HeJ inbred mice. In this experiment, alcohol dependence was induced using an ethanol-vapor exposure protocol shown previously in our lab to generate long-lasting impairment of spontaneous behavioral activity.

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