Date of Thesis


Thesis Type

Honors Thesis (Bucknell Access Only)

Degree Type

Bachelor of Science

First Advisor

Jennie Stevenson

Second Advisor

Judy Grisel


One of the hallmarks of an alcohol use disorder is a disruption in the network of one's social relationships, but the mechanism that underlies this dysfunctional social system is not well understood. There is, however, an extensive body of literature implicating the neuropeptide hormones oxytocin and vasopressin in social behaviors, and alcohol has been shown to alter some of the central and peripheral functions of these neuropeptides. Nonetheless, research has yet to fully investigate the relationship between alcohol, oxytocin, vasopressin, and dysfunctional social systems. This study sought to determine whether chronic alcohol exposure induces disruptions to oxytocin-producing and vasopressin-producing neuronal populations within the paraventricular nucleus of the hypothalamus. All investigations were conducted in prairie voles, a species that forms stable social bonds and willingly consumes high levels of alcohol, which makes them a useful model to examine the influence of alcohol on pro-social neuropeptides. All neurobiological analysis was conducted using immunohistochemistry in order to identify areas of protein expression and cellular activation patterns within the paraventricular nucleus. In order to provide a more comprehensive investigation into the effects of alcohol, this thesis included both voluntary and involuntary methods of alcohol exposure. Within the voluntary model, there were alcohol-treated groups that reflect either continuous or limited access to alcohol, enabling an investigation into whether different patterns of drinking have similar effects on these neuronal populations. Analysis indicated that there was a significant decrease in the number of oxytocin-producing neurons in the Continuous Access group in the anterior region of the paraventricular nucleus. Posterior oxytocin, on the other hand, significantly and negatively correlated to alcohol consumption and preference during social, but not isolated, drinking in the Continuous Access group. With respect to vasopressin, there was a significant decrease in the mean number of vasopressin-producing cells compared to the mean of all control animals that were not exposed to alcohol. Within the involuntary method, this study compared the effects of a single alcohol or saline injection to chronic injections. Analysis revealed a decrease in the activation of oxytocin-producing neurons of the posterior paraventricular nucleus with chronic injections of alcohol. Vasopressin expression was unchanged in response to acute or chronic injections. Taken together, this thesis provides evidence of a complex, region-specific relationship between chronic alcohol and oxytocin-producing neurons in the paraventricular nucleus of the hypothalamus. It also demonstrates that chronic consumption of alcohol can alter the vasopressin-producing neuronal population. With further investigation, this information could help illuminate the biological changes that accompany disrupted social bonds in individuals who misuse alcohol.