The role of endogenous opioids in the blockade of reproductive function in the rat following exposure to acute stress.

The present experiments investigated the involvement of endogenous opioids in the preovulatory disruption of luteinizing hormone release and ovulation following exposure to an acute stressor. The effect of exposure to an acute stressor and/or treatment with naloxone hydrochloride on the proestrus/estrus display of lordosis behavior is also reported. Electric shocks (2 mA) delivered at 10-min intervals for three hours during the period of the preovulatory luteinizing hormone surge in adult cyclic female rats resulted in the blockage of luteinizing hormone release, decreased lordosis behavior, and inhibition of ovulation. The anti-luteinizing hormone and anti-ovulatory actions were antagonized by the administration of naloxone hydrochloride shortly prior to the application of the stressor, which suggests that the observed blockage of ovulation is mediated by endogenous opioids known to be elevated in response to a stressor. It is argued that the most likely mechanism by which endogenous opioids inhibit luteinizing hormone release and ovulation is by inhibiting luteinizing hormone releasing hormone release, and/or decreasing its production in the hypothalamus. In contrast, naloxone only partially antagonizes the anti-lordotic actions of electric shock. It is therefore further argued that the inhibition of luteinizing hormone release alone is not sufficient to explain the dramatic decrease in lordosis behavior observed following exposure to an acute stressor. Adrenal progesterone released in response to adrenocorticotropic hormone release following exposure to an acute stressor, in association with inhibited luteinizing hormone releasing hormone release is hypothesized to be responsible for the observed decrease in lordotic behavior, and the inhibition of luteinizing hormone release.