Physiologic stress elicits impairment of reproductive function, in part, by the suppression of luteinizing hormone (LH) secretion. Two populations of kisspeptin-synthesizing neurons in the hypothalamus play essential roles in controlling the pulsatile and surge modes of LH secretion and are potential direct targets of stress-activated neural circuits; however, the mechanism(s) for impairment of kisspeptin cells during stress remain unclear. Here, we conducted four experiments to test the hypothesis that corticotropin releasing hormone receptor 2 (CRHR2) signaling contributes to impaired pulsatile and surge LH secretion via direct actions upon kisspeptin cells.
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