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

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% (