Affiliation: College of Arts and Sciences, Department of Biology
According to the Centers for Disease Control, excessive alcohol use cost the United States nearly 249 billion dollars in 2010 and binge drinking accounted for 77% of these costs. Repeated episodes of binge drinking may increase the risk of alcohol use disorder and thus, it is important to understand the neurobiological changes that occur with excessive alcohol drinking. Individuals struggling with alcohol substance-use disorder have an upregulation of the neuropeptide, dynorphin, in the hippocampus. Dynorphin, the endogenous ligand for the Kappa Opioid Receptor, is known to produce negative affective states in humans. Due to the likely presence of dynorphin upregulation following binge drinking, alcohol drinking experiments were conducted via the drinking in the dark (DID) paradigm. Dynorphin knockout was performed in a model of binge-like drinking to gain insight on the role of dynorphin in mediating alcohol consumption behaviors. Since a history of alcohol drinking can increase anxiety, and knockout animals consumed less ethanol than control animals, an elevated plus maze (EPM) was used to examine whether the knockout alters anxiety-levels in ethanol treatment and naïve (non-drinking) animals. The results demonstrate the effects of dynorphin knockout on ethanol consumption behaviors. Experiments demonstrated that the dynorphin knockout cohort had lower ethanol consumption levels. In addition, the ethanol treatment mice did not demonstrate significant changes in anxiety-like behavior compared to the naïve mice. Understanding these neurobiological changes can help advance the range of pharmaceutical medications for substance-use disorders.