Abstract
Development of post-stress depression in rats was accompanied by long-term moderate activation of the expression of transcription factor c-Fos in the neocortex, hippocampus, and paraventricular nucleus of the hypothalamus. Hypoxic preconditioning preventing depressive state in rats under conditions of unavoidable stress considerably enhanced c-Fos expression in the studied brain regions during the early stages of stress response (days 1-5) and promoted its normalization at later terms (10 days). Disturbances in the wavy dynamics of c-Fos expression can contribute to the pathogenic mechanisms of depression, in particular and induce hyperproduction of hypothalamic neurohormone corticoliberin, whereas potentiation of early expression of this factor in response to stress is obviously necessary for prevention of post-stress disorders.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have