Modulation of lordosis behaviour in the female rat by corticotropin releasing factor, beta-endorphin and gonadotropin releasing hormone in the mesencephalic central gray.

A possible functional relationship between corticotropin-releasing factor (CRF) and opiate peptide neuronal systems (beta-endorphin, dynorphin1-17 and Met-enkephalin) and their interactions with gonadotropin releasing hormone (GnRH) in the mesencephalic central gray (MCG) for the regulation of lordosis behaviour was assessed in ovariectomized, oestrogen-treated and oestrogen-progesterone-treated female rats. Lordosis behaviour triggered by male mounting was inhibited in a dose-dependent fashion by CRF microinfused into the MCG in both oestrogen-treated and oestrogen-progesterone-treated female rats. This CRF-induced inhibition of lordosis could be overcome by a pre-infusion of naloxone or anti-beta-endorphin-globulin (anti-beta-end-G) directly into the MCG but not by anti-Met-enkephalin globulin (anti-enk-G) or anti-dynorphin1-17 globulin (anti-dynor-G). Supporting data indicate that the facilitation of lordosis behaviour induced by treatment with naloxone or anti-beta-end-G alone but not with anti-enk-G or anti-dynor-G may be due to enhanced GnRH release. This results from the action of these substances in overcoming the inhibition of GnRH secretion mediated specifically by beta-endorphin but not by Met-enkephalin or dynorphin1-17 in the MCG. These studies together with previous data showing that GnRH can overcome the abolition of lordosis by beta-endorphin in the MCG, indicate a close relationship between beta-endorphin (but not Met-enkephalin or dynorphin) and GnRH systems in the MCG in the control of lordosis behaviour. Thus, the inhibition of lordosis by CRF and the complete reversal of this blockade by naloxone or anti-beta-end-G may suggest that CRF could enhance the release of beta-endorphin from fibres in the MCG; beta-endorphin then inhibits lordosis by inhibiting the release of GnRH. However, a direct inhibitory effect of CRF on GnRH release is also likely since anti-CRF-gamma-globulin (anti-CRF-G) infused into the MCG produced a long-lasting facilitation of lordosis which can be blocked by an antagonist analogue of GnRH; in addition, previous studies have shown that GnRH infused into the MCG completely overcame the CRF-induced abolition of lordosis and potentiated lordosis to high levels. These results suggest that there may be functional neuroanatomical relationships between CRF, beta-endorphin and GnRH neuronal systems in the MCG in the control of female sexual behaviour. Neither Met-enkephalin nor dynorphin1-17 appear to participate in such mechanisms.