Description:

Abstract:

Stress is a significant risk factor for the development, and exacerbation, of numerous psychiatric disorders, including major depressive disorder (MDD). The glucocorticoid corticosterone (cortisol in humans; CORT) is the primary ‘stress hormone’ in the body. In MDD, normal circadian rhythms of high and low CORT are flattened, leading to dysregulated and chronically elevated levels. Previous studies have found that static, chronically elevated levels of CORT induce anxiety-like behavior and impair reward-guided operant behaviors, but have only reported effects on male mice. We explicitly compared male and female mice and found that the effects occur exclusively in male mice. We are exploring the reasons for this sex difference in CORT-induced behavioral changes, which may be due to differences in CORT metabolism. In male mice, we have elucidated a connection between CORT signaling and dopamine transmission occurring through regulation of dopamine reuptake. I will describe our current model for glucocorticoid regulation of dopamine circuit function and discuss future directions, which are open to feedback.

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