Title

Chronic intermittent ethanol exposure lowers brain corticosterone levels in male C57BL/6J mice

Faculty Mentor

Dr. Antoniette Maldonado-Devincci

Department

Biology

Document Type

Poster

Publication Date

Spring 2019

Abstract

Alcoholism and withdrawal can seriously affect the brain, including altering regulation of steroids and hormones. Neuroactive steroids are important for learning, memory and stress responses. Previous research showed that acute ethanol exposure increased hippocampal levels of the neuroactive steroid corticosterone, but not allopregnanolone (3α,5α-THP). Corticosterone and 3α,5α-THP are both progesterone-derived neurosteroids. Based on this, we hypothesized that chronic intermittent ethanol would induce compensatory increases in corticosterone in the same brain regions where we previously observed decreased 3α,5α-THP. The present study examined how chronic intermittent ethanol exposure altered brain corticosterone levels in subregions of the nucleus accumbens, amygdala, and hippocampus. Male C57BL/6J mice were exposed to four cycles of chronic intermittent ethanol vapor or air over four weeks. Eight hours following the last ethanol-vapor or air exposure cycle, mice were euthanized, brains collected, cut into 40 μm sections, and immunohistochemical analysis was conducted to visualize brain corticosterone immunostaining. Data indicate that corticosterone immunostaining was increased by 31.0±13.8% (p<0.02) in ethanol-exposed mice compared to air-exposed controls in the nucleus accumbens core. However, no change was observed in the nucleus accumbens shell. In the lateral subregion of the amygdala, there was a 22.1±12.0% (p<0.05) decrease in corticosterone immunostaining in ethanol-exposed mice compared to air-exposed mice. However, there was no change in the basolateral or central nucleus subregions of the amygdala. In the CA3 subregions of the hippocampus, corticosterone immunostaining was decreased by 21.44±12.2% in ethanol-exposed mice, but no change in the CA1 subregion of the hippocampus. Together, in the present work we observed compensatory changes in corticosterone responding in the nucleus accumbens core and in the CA3 subregion of the hippocampus. However, in the lateral amygdala we observed a decrease in both corticosterone in the present work and 3α,5α-THP in previous work. These data indicate specific subregions of limbic brain structures show compensatory changes in corticosterone levels, where we previously observed changes in 3α,5α-THP. Currently, other limbic brain structures and a longer withdrawal time point are under investigation for assessment of changes in brain corticosterone levels following chronic intermittent ethanol exposure.

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