Endogenous opioid control of pulsatile LH secretion in rams: modulation by photoperiod and gonadal steroids

The role of endogenous opioid peptides in the inhibitory control of pulsatile LH secretion was studied in adult Soay rams at different stages of the seasonal reproductive cycle, entrained by an artificial lighting regimen of alternating 16-week periods of long and short days. The LH responses to the acute administration of naloxone (opioid antagonist) and morphine (opioid agonist) were measured in intact rams (n = 7), testosterone-implanted castrated rams (n = 8) and castrated rams (n = 8) to assess the interaction between photoperiod and gonadal steroids in the opioid control of LH secretion. In the intact and testosterone-implanted castrated rams, naloxone (1.7 mg/kg i.v.) increased and morphine (1.0 mg/kg i.v.) decreased mean LH concentrations and LH pulse frequency during the sexually active phase under short days, but these effects were reduced or absent during the inactive phase under long days. The changes in the LH responses occurred in close parallel with the photoinduced changes in endogenous LH secretion. In the castrated rams receiving no supplementary testosterone, plasma LH concentrations were permanently raised and there were only minor changes related to the photoperiod. Naloxone (1.7 mg/kg) induced transient increases in LH secretion at all stages, and morphine (1.0 mg/kg) failed to suppress LH levels under both short and long days. LHRH stimulation tests revealed that there were changes in LH release related to the induced reproductive cycle in the intact and testosterone-implanted rams but not in the castrated rams; these changes in the responsiveness of the pituitary gonadotrophs to LHRH could not account for the changes in the LH response to the opiate drugs. These results illustrate that an endogenous opioid mechanism is involved in the tonic inhibition of LH secretion acting to regulate the pulsatile release of LHRH from the hypothalamus. This system can be shown to be functional in a steroid-dependent manner in the sexually active phase of the seasonal cycle, but not in the inactive phase of the cycle when non-opioidergic mechanisms are presumed to predominate in the inhibition of LH secretion.