Regulation of prolactin release by endogenous opiates

Abstract

ENDORPHINS, the endogenous peptides recently isolated and identified in brain have been implicated in regulation of pain^1–4. But their wide distribution throughout the brain^5–7 and their profound behavioural effects after central administration⁸ suggest an involvement in other central nervous system processes. Immunohistochemical identification of these endorphins (refs 9, 10 and F. Bloom, personal communication) in hypothalamic neurones indicated that neuroendocrine effects are probable. Morphine was previously reported to block ovulation, while more recently, morphine¹¹ and endorphins^12–14 were observed to stimulate release of prolactin and growth hormone. Yet, these observations have not established a direct, tonic participation of endorphins in hypothalamic and anterior pituitary function. The absence of any direct action of opiate antagonists has been taken as an argument against any tonic role of endorphins. Recent reports indicate, however, that opiate antagonists do modify on-going central processes. For example, naloxone and naltrexone lower pain threshold in appropriate conditions in man and experimental animals^15–18. Using naltrexone as a tool to block opiate receptor function, we have explored whether endorphins are tonically involved as a putative neurotransmitter in the regulation of prolactin release. The results presented here demonstrate a new instance where an opiate antagonist modifies normal function. The data agree with a preliminary report indicating that naloxone reduced prolactin release in immature female rats¹⁹.