Assessment of GABAA α1, α4, and α5 receptor subunit protein expression in dorsal and ventral hippocampus of adult male and female Long-Evans rats after moderate prenatal alcohol exposure.

Fetal Alcohol Spectrum Disorders (FASD) describe a range of neurobiological and behavioral changes following prenatal alcohol exposure. Previous work has shown that moderate prenatal alcohol exposure (mPAE) can produce alterations to GABAergic neurotransmission in the hippocampal formation (HPF) as well as morphological alterations in GABAergic interneuron expression in adult rats. In the present study, we tested the hypothesis that mPAE differentially alters GABAA subunit protein expression in dorsal and ventral HPF of naïve adult male and female Long-Evans control and mPAE rats. We focused our attention on the α1, α4, and α5 subunits as they have relatively high densities within the hippocampus and have been linked to hippocampal-dependent learning and memory. Membrane fractions were collected from dorsal and ventral HPF, and western blots were performed to detect levels of GABAA α1, α4, and α5 subunit protein expression. Overall, we did not detect prenatal treatment group differences suggesting that mPAE does not result in differential GABAA subunit protein expression in dorsal or ventral HPF of male and female rats. However, the results revealed significantly greater protein expression for α4 and α5 subunits in the dorsal HPF. GABAA α1 protein expression did not vary significantly across the dorsal and ventral HPF. Our findings support the general conclusion that GABAA subunit protein expression in the HPF reflects intrinsic regional specialization of GABAergic signaling rather than effects of mPAE.