Modulation of Endogenous Opioid Influence on Luteinizing Hormone Secretion by Progesterone and Estrogen*

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Abstract
Studies were undertaken using the opiate receptor antagonist naloxone (NAL) to evaluate the relative influence of endogenous opioid peptides (EOP) on LH [luteinizing hormone] secretion in cycling and ovariectomized, steroid-treated adult rats. Intact animals received NAL (2 mg/kg, s.c.) or saline (control vehicle) at 0800 and 1400 h on estrus, 0800 h on diestrus day 1, 2000 h on diestrus day 2, and before (at 0800, 1200 and 1400 h) and during the preovulatory LH surge (at 1600 and 1800 h) on proestrus. NAL stimulated LH release by 2- to 3-fold at all stages of the estrous cycle, including during the proestrous gonadotropin surge. Ovariectomized rats were treated with estradiol benzoate (EB; 7.5 .mu.g/rat, s.c.) and 2 days later received NAL (2 mg/kg, s.c.) or saline at 1000, 1200, 1400, 1600 and 2000 h. NAL induced a relatively small (44-73%), but significant, increase in LH release before (1000, 1200 and 1400 h), during (1600 h) and after (2000 h) the afternoon LH rise. While progesterone (P) treatment (5 mg, s.c., day 2 at 1000 h) of EB-primed ovariectomized rats augmented NAL-induced LH release before the LH surge (1200 h), it abolished the LH secretory response to NAL during the LH surge (1400, 1600 and 1800 h). The NAL-induced LH response returned after the LH surge at 2000 h. Likewise, administration of P on proestrus morning (0900 h) abolished the LH secretory response to NAL during the LH surge. Central opioid neurons participate in the tonic inhibition of LH secretion at all stages of the estrous cycle of the rat. The ability of exogenous P to advance and amplify the LH surge on proestrus, and in EB-primed ovariectomized rats appears to result in part from a reduction in the EOP inhibitory influence on LH secretion and may indicate a role for EOP in mediating the stimulatory effects of endogenous steroids on LH secretion the female rat.