Adolescent Alcohol’s Effects on Adult Drinking and Somatostatin Neurons
Open Access
- Author:
- Springer, Matthew
- Area of Honors:
- Biology
- Degree:
- Bachelor of Science
- Document Type:
- Thesis
- Thesis Supervisors:
- Nikki Crowley, Thesis Supervisor
Sarah Mary Assmann, Thesis Honors Advisor - Keywords:
- Somatostatin
Neurodevelopment
Alcohol Consumption - Abstract:
- Adolescence serves as a vital period of brain development. Reorganization of the prefrontal cortex is one of the most important and prominent biological changes during this time. In this region, the subclass of neurons expressing somatostatin play an important role. These adolescent brain changes lead to complex changes in behavior, particularly in the area of risk-taking. These effects have been shown to be modulated by substances such as alcohol, which is one of the most prevailing substances of abuse in society today. The effects of alcohol on brain circuitry are often modeled in mice, as in this research. Alcohol is most dangerous when consumed in high quantities, such as during bouts of binge drinking. Literature in humans and animal models has shown that adolescent exposure to alcohol generally increases alcohol consumption in adulthood. Other literature has shown that SST neurons in the prelimbic cortex are implicated in binge drinking behavior. This thesis examines the effects of adolescent alcohol exposure in mice through a Drinking in the Dark (DID) model before repeating the DID model in adulthood or diverting mice into an alternative 2 Bottle Choice (2BC) model. Electrophysiology at the time of adult exposure was conducted to examine the intrinsic excitability of SST neurons in the prelimbic cortex prior to adult alcohol exposure in adolescent exposure mice. Results showed that SST neurons in the prelimbic cortex were hyperexcitable at the time of adult drinking models in adolescent start drinking mice. No discernible changes were seen in the DID and 2BC models between mice that began drinking in adolescence and mice that began drinking in adulthood. Taken together, this suggests that in mouse models, biological adaptations driven by adolescent alcohol consumption do not drive increased consumption of alcohol in adulthood, and other social and environmental factors should be considered in humans.