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Journal of Undergraduate Research

Keywords

chronic ethanol, GABA(A), VTA, excessive alcohol

College

Family, Home, and Social Sciences

Department

Psychology

Abstract

The Centers for Disease Control and Prevention attributes approximately 80,000 deaths annually to excessive alcohol use (CDC), and alcohol consumption is the third leading cause of preventable deaths in the United States (Mokdad et al., 2004). These statistics do not even describe the detrimental effects alcohol addiction has on personal lives and families. The accepted model for addiction in the brain is a change in the normal regulation of the neurotransmitter dopamine (DA) in the mesolimbic pathway. Studying this pathway is important in developing treatments for addiction, which has implications to improve the lives of many suffering people. The primary areas involved include the ventral tegmental area (VTA) in the midbrain and the nucleus accumbens (NAc). Dopamine neurons in the VTA are primarily regulated by inhibitory gamma-aminobutyric acid (GABA) neurons also located in the VTA. The GABA(A) receptor on VTA GABA neurons normally allows negatively charged chloride ions into the cell, hyperpolarizing it, which leads to inhibition of the excitability of the neuron. Others have shown in opiate-dependent animals that GABA(A) receptors switch their function from being inhibited by GABA to being excited (Vargas-Perez et al., 2009). We show that the change in DA regulation due to alcohol dependence occurs because of a switch in function of the GABA(A) receptors on GABA neurons in the VTA.

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