Collections > UNC Chapel Hill Undergraduate Honors Theses Collection > Quantification of Interneuron Damage in a Mouse Model for Prenatal Alcohol Exposure

Prenatal alcohol exposure (PAE) can result in a range of mental disabilities and physical defects. Because adults affected by PAE demonstrate increased susceptibility to alcohol dependence, it was hypothesized that PAE leads to the loss of inhibitory GABAergic interneurons in corticostriatal circuits that regulate reward perception. Offspring of mice that experienced acute ethanol exposure on gestation day 7 (GD 7) were used as an animal model. Intracranial self-stimulation studies showed a marked difference in threshold for non-exposed controls and PAE mice during the first 15 minutes following morphine injection, but no significant difference was shown with alcohol or cocaine. Immunohistochemistry against parvalbumin was performed to visualize the GABAergic interneurons of the CNS in the nucleus accumbens, medial prefrontal cortex, dorsal striatum, and medial septum. A preliminary count of the interneurons in the nucleus accumbens showed no difference between control and PAE mice. In the future, further quantification of GABAergic interneurons in all four regions of interest may conclude that maternal ethanol ingestion on GD 7 causes significant damage to the normal distribution of inhibitory interneurons in CNS structures associated with reward perception.