Modulation of lordosis behavior of female rats by naloxone, beta-endorphin and its antiserum in the mesencephalic central gray: possible mediation via GnRH.

D J Sirinathsinghji

Index: Neuroendocrinology 39(3) , 222-30, (1984)

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Abstract

The role of endogenous opiate peptides in the mesencephalic central gray (MCG) and their possible interactions with gonadotropin-releasing hormone (GnRH) in the regulation of lordosis behavior was assessed in ovariectomized, estrogen-treated and estrogen-progesterone-treated female rats. Lordosis behavior triggered by male mounting was enhanced by microinfusion of naloxone and anti-beta-endorphin-globulin (anti-beta-end-G) but not by anti-met-enkephalin-globulin or anti-dynorphin-globulin into the MCG in both estrogen-treated and estrogen- (low dose) progesterone-treated females. The potentiating effects of naloxone and anti-beta-end-G could be blocked by a preinfusion of either anti-GnRH-globulin or an antagonist analog of GnRH directly into the MCG. However, two potent antagonist analogs of GnRH were not effective in blocking lordosis indicating a dissociation between their neural actions and their known inhibitory effects on luteinizing hormone release. Conversely, beta-endorphin but not met-enkephalin or dynorphin infused into the MCG inhibited lordosis behavior in both estrogen-treated and estrogen-progesterone-treated rats. This beta-endorphin-induced inhibition of lordosis in the estrogen-treated rats could be overcome by GnRH microinfused directly into the MCG which potentiated lordosis to high levels. These observations provide evidence that beta-endorphin may be the sole opiate peptide in the MCG involved in the control of lordosis behavior and also suggests a functional relationship with GnRH systems in the MCG in such a regulatory mechanism.