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The effects of long-term anesthesia with methoxyflurane on plasma LH and prolactin concentrations were compared to those induced by exposure to ether. Methoxyflurane significantly decreased prolactin levels and had a slight effect of LH, whereas ether produced an important release of prolactin without affecting LH.

Luteinizing hormone-releasing hormone (LHRH) and somatostatin (SRIF) release was assessed in superfused slices of mediobasal hypothalamus. Release of both neurohormones by depolarizing agents (K+, 56mM ; veratridine, 50 muM) was shown to be Ca2+-dependent, according with the stimulus-secretion coupling hypothesis. Opiates (beta endorphin, 10(-7)M and D-ALA2-Met-enkephalinamide 10(-7)M) did not alter the spontaneous release of LHRH and SRIF, but inhibited significantly the K+-induced neuropeptide release. The effect was reversed by the opiate antagonist naloxone (10(-7)M), while naloxone was ineffective by itself. Vasoactive intestinal peptide (VIP 10(-9)M) significantly inhibited K+ evoked release of SRIF ; LHRH release was unaffected. The effect of VIP on SRIF release was dose-dependent ; secretin, a partial VIP agonist, was also active at higher doses. The data suggest that : 1) opiates, acting through specific opiate receptors located on LHRH and SRIF neurons, modulate the release of the neurohormones ; 2) the inhibitory effect of opiates could be due to an inhibition of calcium influx through voltage-dependent calcium channels ; 3) this interaction may account for the stimulation of growth hormone and the inhibition of luteinizing hormone observed after systemic administration of opiates ; 4) VIP inhibits SRIF release, by acting on VIP receptors present on MBH SRIF terminals ; the effect is consistent with the stimulation of GH reported after in vivo administration of the peptide.

An experimental increase in serotonin (5-HT) induced shortly before the "critical period" of ovulation control blocks the release of LH. Administration of a synthesis inhibitor of the amine p-chlorophenylalanine, (pCP) is ineffective when given during the critical period. However, pCP given in the evening of dioestrus II (18 to 24 hours before the "critical period") blocks ovulation. That 5-HT is specifically involved in this delayed effect of the drug is shown by the ability of increasing doses of 5-hydroxytryptophane (5-HTP) to induce with pCP a graded restoration of LH release when given together. This result, obtained in immature rats, has been confirmed in cyclic ones. A positive, permissive effect of 5-HT containing neurons on neural processes leading to LH release and ovulation is thus postulated. This action affects early stages of the LH release regulating mechanisms, in contrast to the classically described inhibiting effect of the amine, which blocks the actual release of LH-RH at the median eminence level during the critical period.