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Journal of Undergraduate Research

Keywords

plasticity, glutamate neurotransmission, midbrain GABA, neurons, ethanol

College

Family, Home, and Social Sciences

Department

Psychology

Abstract

The aim of my ORCA grant was to better under the addictive pathway of ethanol (EtOH) in the ventral tegmental area (VTA) of the brain. The VTA contains several neuron types that release different neurotransmitters, but the type I experimented with was γ-Aminobutyric acid (GABA), which is the primary inhibitory neurotransmitter in the brain. GABA neurons regulate dopamine (DA) neurons in the VTA by inhibiting DA release but when the GABA neurons are inhibited, DA neurons are hyperexcitable and therefore have an increased DA release in the VTA. I originally sought out to see if nicotinic acetylcholine receptors (nAChRs) present on GABA neurons in the VTA is where EtOH is known to act (Davis and de Fiebre). Specifically I suspected that the nAChR subunit α-7, may be the leading mechanism of action of EtOH in the VTA. From previous experimentation in Dr. Steffensen’s lab, it was found that GABA neurons in the VTA are experiencing plasticity – changes in neuronal behavior – when exposed to only one injection of EtOH. I hypothesized that plasticity occurring in VTA GABA neurons could be blocked by the α-7 nicotinic antagonist methyllycaconitine (MLA).

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