INVOLVEMENT OF CORTICOTROPIN-RELEASING HORMONE AND ENDOGENOUS OPIOID-PEPTIDES IN PROLACTIN-SUPPRESSED GONADOTROPIN-RELEASING-HORMONE RELEASE IN-VITRO

Corticotropin-releasing hormone (CRH) has been shown capable of inhibi ting hypothalamic gonadotropin-releasing hormone (GnRH) release throug h activation of an endogenous opioid peptide (EOP)-dependent mechanism . Recently, we have shown that prolactin (PRL) stimulates CRH release and inhibits GnRH release by hypothalami explanted from male rats. Thu s, the present study was undertaken to investigate whether the inhibit ory effect of PRL on GnRH release in vitro is mediated by CRH and/or E OP. To this aim, the release of GnRH in response to PRL was evaluated in presence of CRH(9-41) alpha-helical (CRH(9-41)), a CRH receptor ant agonist, and/or naloxone (NAL), a nonselective opioid receptor antagon ist, using a static hypothalamic organ culture system which enabled us to evaluate immunoreactive GnRH (iGnRH) release from individually inc ubated longitudinally halved hypothalamic. As previously shown, PRL at the concentration of 100 nmol/l inhibited basal iGnRH release by abou t 35 %. CRH(9-41) or NAL overcame the inhibitory effect of PRL on iGnR H release in a concentration-dependent fashion. The simultaneous co-in cubation with both antagonists was not more effective than each single antagonist. CRH(9-41) did not have any effect on basal iGnRH release whereas NAL, as previously reported, increased it. In addition, PRL at the concentration of 100 nmol/l stimulated basal hypothalamic beta-en dorphin (beta-EP) release. In conclusion, these data show that antagon ism to CRH receptors counteracts the suppressive effects of PRL upon G nRH release and that PRL, is able to stimulate hypothalamic beta-EP re lease in vitro.