Naloxone blocks the effects of delta 9-tetrahydrocannabinol on serum luteinizing hormone and prolactin in rats.

The present study was undertaken to determine if the effects of delta 9-tetrahydrocannabinol on gonadotropin secretion are mediated through endogenous opioid neurons in the rat. Ovariectomized rats were treated with estradiol-benzoate (EB, day O) and with progesterone (P) at 11:00 h on day 2. At 13:00 h (day 2), these estradiol primed and progesterone-treated (EBP) animals received either delta 9-THC (3mg/kg in oil, i.m.); naloxone (Nal) 3 mg/kg in saline, s.c.) or delta 9-THC + Nal. All animals were decapitated at 16:00 h and trunk sera were assayed for luteinizing hormone (LH) and prolactin (Prl), while medial basal hypothalami (MBH) were assayed for luteinizing hormone-releasing hormone (LHRH). Naloxone enhanced the EBP-induced hypersecretion of LH by 2-fold while delta 9-THC completely blocked the EBP-induced secretion of LH. delta 9-THC slightly diminished the stimulatory effect of Nal on LH secretion and caused a 2-fold increase in serum Prl concentrations, while Nal did not influence the serum PRL levels in these EBP rats. However, Nal did block the stimulatory effects of delta 9-THC on Prl secretion. delta 9-THC caused a significant increase in MBH content of LHRH, an effect which was prevented by Nal. These results suggest that the inhibitory effects of delta 9-THC on serum LH and the stimulatory effect of the cannabinoid on Prl are mediated by an opioid mechanism.