Effects of Beta‐Endorphin on Pulsatile Luteinizing Hormone and Prolactin Secretion During the Follicular Phase in the Ewe

Abstract

Abstract The present study was undertaken to determine the effects of the endogenous opioid ligandbeta-endorphin on pulsatile luteinizing hormone (LH) secretion and plasma prolactin concentrations during the follicular phase of the ewe. Oestrous cycles were synchronized by injection of prostaglandin analogue and, commencing 13 h later, saline or beta-endorphin (2, 10 or 50 mug) was injected intracerebroventricularly at hourly intervals for 3 h. Treatment with beta-endorphin was followed by a significant reduction in LH pulse frequency at all doses due to almost complete cessation of pulses. There were no significant changes in LH pulse amplitude or mean LH concentrations. At the lowest dose ofbeta-endorphin, LH pulses recommenced within 3 h of the last injection in all animals and pulse frequency was not significantly different from the saline-injected controls during the 3 h post-treatment period. Following treatment with 10 or 50 mug beta-endorphin, LH pulse frequency remained suppressed during the 3 h post-treatment period but was not different from saline-treated controls on the following day. The time to the onset of the LH surge was not affected by intracerebroventricularbeta-endorphin. Plasma prolactin concentrations were significantly increased following intracereb-roventricular injection of 10 or 50 mug beta-endorphin, declining to control values soon after treatments stopped. Intravenous administration of 50 mug beta-endorphin had no effect on LH but was accompanied by a small increase in prolactin concentrations. While these results indicate that hypothalamicbeta-endorphin may be involved in the central control of LH and prolactin secretion, they provide no evidence for subtle modulation of LH pulse frequency by this neuropeptide.