Examining mechanisms by which acute psychosocial stress disrupts the proestrous LH surge and ovulation in female mice.

Stress most often inhibits reproduction. Exposure to an acute layered psychosocial stress paradigm (ALPS) on proestrus disrupts the LH surge in 60% to 70% of adult female mice without interfering with the progression of the estrous cycle. The present study aims to expand on these observations by investigating effects of ALPS exposure on ovulation and potential mechanisms involved in surge disruption. The most common response to ALPS exposure was disruption of the LH surge and blockade of ovulation; however, in some mice in which no LH surge was detected, ovulation did occur. Factors from the adrenal cortex and medulla, corticosterone and catecholamines (norepinephrine and epinephrine), respectively, are increased during stress; we thus tested whether these factors mediate the effects of stress on the LH surge and ovulation by applying ALPS in adrenalectomized (ADX) animals. ADX did not reverse the disruptions of the LH surge/ovulation after ALPS. Further studies aimed to investigate potential roles of individual adrenal factors in this response. We tested whether administering corticosterone, in the absence of stress, was sufficient to suppress the LH surge and ovulation. It was not. Finally, we tested whether blockade of β-adrenergic signaling during ALPS would rescue the LH surge and/or ovulation. Propranolol, a nonselective β-adrenergic receptor blocker, given 1 hour before ALPS failed to reverse the disruptive effects of stress. Together, these data confirm the effectiveness of ALPS in disrupting both the LH surge and ovulation. They further indicate that the adrenal gland is dispensable for these effects.