Interaction between opioid peptides and monoamines in the regulation of gonadotropin secretion in the female rat.

Abstract

AbstractAdult female rats were injected with 15 μg β‐endorphin twice, at 12: 00 and 15: 00, on the day of proestrus, with or without pretreatment with the antiserotonergic drug p‐chlorophenylalanine (PCPA, 300 mg/kg) or the anticholinergic drug atropine sulfate (150mg/kg). Administration of β‐endorphin alone caused a slight decrease in pre‐ovulatory LH release and blocked ovulation in 4 of the 10 animals. Pretreatment with PCPA, but not atropine, completely blocked the β‐endorphin action. Injection with naloxone (2 mg/kg) induced a significant increase in serum LH levels 60 minutes later in immature female rats. The naloxone‐induced LH rise was reduced by concomitant intraperitoneal administration of β‐endorphin (200 μg/kg). This β‐endorphin inhibition of naloxone action was, however, completely abolished by pretreatment with PCPA, while PCPA showed a tendency to potentiate the LH response to naloxone alone. These results suggest that serotonergic systems participate in the mechanisms whereby β‐endorphin suppresses LH secretion. In addition, the stimulatory action of naloxone on LH secretion was markedly suppressed when reserpine (2 mg/kg) or phenoxybenzamine (20 mg/kg), all antinoradrenergic drugs, were first administered, suggesting that the naloxone action to promote LH release is mediated in part via hypothalamic noradrenergic systems.