Robert Cohoon and Dr. Scott Steffensen, Department of Psychology
The rationale for this study was predicated on the belief that advancement in the understanding of the brain mechanisms underlying the recreational use and abuse potential of drugs will pave the way for more effective treatment strategies that would save lives and resources throughout the world. Each year more people are enslaved by addiction. It can range from alcohol and illicit drugs from the street to milder stimulants such as coffee or non-prescription drugs. Regardless of the drug, the brain’s chemistry is influenced by these chemicals. This study has hit especially close to home with me because I have a brother that has been enslaved by addiction for twenty years. I have considered this project a service to my brother.
We had previously demonstrated that VTA GABA neuron (inhibitory brain cells) firing rate is inhibited by acute alcohol and adapts to chronic alcohol treatment, and that electrical coupling between VTA GABA neurons is suppressed by ethanol. We hypothesized that GABA neurons in the VTA may be critical neuronal substrates along the continuum of alcohol intoxication, reinforcement, and dependence. Although we had previously characterized the effects of ethanol on mouse VTA GABA neurons we didn’t know the role the GABA(A) receptor plays in these effects. I proposed to study the effects of the selective GABA(A) antagonist Ro 15-4513 on VTA GABA neuron firing rate with acute ethanol.
We evaluated the effects of intraperitoneal injections of both Ro 15-4513 (1.0-3.0g/kg) and ethanol (0.2-2.0 g/kg) on firing rate. Although the research is ongoing and will not be complete until next semester it seems that the data is going to show that this specific GABA(A) receptor does indeed play a role in intoxication of mice. This is good news because we are laying the foundation for future studies of ethanol in mice. This project will be completed and a poster will be presented at the Society for Neuroscience later this year.