OPIOID MODULATION OF GONADOTROPIN-RELEASING-HORMONE RELEASE FROM THE HYPOTHALAMIC PREOPTIC AREA IN THE PIG

Two experiments (Exp) were conducted to examine in vitro the release of gonadotropin releasing hormone (GnRH) from the hypothalamus after treatment with naloxone (NAL) or morphine (MOR). In Exp 1, hypothalamic-preoptic area (HYP-POA) collected from 3 market weight gilts at sacrifice and sagittally halved were perifused for 90 min prior to a 10 min pulse of morphine (MOR; 4.5 x 10(-6) M) followed by NAL (3.1 x 10(-5) M) during the last 5 min of MOR (MOR + NAL; n=3). The other half of the explants (n=3) were exposed to NAL for 5 min. Fragments were exposed to KCl (60 mM) at 175 min to assess residual GnRH releasability. In Exp 2, nine gilts were ovariectomized and received either oil vehicle im (V; n=3); 10 mu g estradiol-17 beta/kg BW im 42 hr before sacrifice (E; n=3);.85 mg progesterone/kg BW im twice daily for 6 d prior to sacrifice (P-4; n=3). Blood was collected to assess pituitary sensitivity to GnRH (.2 mu g/kg BW) on the day prior to sacrifice. On the day of sacrifice HYP-POA explants were collected and treated as described in Exp 1 except tissue received only NAL. In Exp 1, NAL increased (P<.05) GnRH release. This response to NAL was attenuated (P<.05) by coadministration of MOR. Cumulative GnRH release after NAL was greater (P<.05) than after MOR + NAL. All tissues responded similarly to KCl with an increase (P<.05) in GnRH release. In Exp 2, pretreatment luteinizing hormone (LH) concentrations were lower (P<.05) in E gilts compared to V and P-4 animals with P-4 being lower (P<.05) than V gilts. LH response to GnRH was lower (P<.05) in E pigs than in V and P-4 animals, while the responses was similar between V and P-4 gilts. NAL increased GnRH release in all explants, whereas, KCl increased GnRH release in 6 of 9 explants. These results indicate that endogenous opioid peptides may modulate in vitro GnRH release from the hypothalamus in the gilt.