Janik, J., Callahan,P. and Rabii, J. (1992). The role of the mu1 opioid receptor subtype in the regulation of prolactin and growth hormone secretion by beta-endorphin in female rats: studies with naloxonazine. JOURNAL OF NEUROENDOCRINOLOGY 4(6): 701-708. The mu opioid receptor subtype has been reported to mediate the prolactin secretory response to opioids. This receptor subtype has been implicated in the morphine-induced prolactin increase, as well as the prolactin response to mu-specific opioid peptides. Subtypes of the mu receptor have been proposed and the mu1 site has been postulated as the receptor subtype involved in the morphine-induced prolactin secretory response. However, the role of this receptor subtype in mediating the endocrine effects of the endogenous opioid peptides has not been characterized. In order to determine the physiological significance of this receptor subtype, animals were pretreated with saline, WIN 44,441-3 (a mu, delta and kappa antagonist) or naloxonazine (a mu1 antagonist) followed by a stimulatory dose of morphine or beta-endorphin. A dose response study for beta endorphin was conducted to detrmine the minimal stimulatory dose of beta endorphin on the prolactin and growth hormone (GH) secretory response. The dose response study indicated that beta-endorphin is a more potent stimulus for prolactin release than for GH. A dose as low as 25 ng increased prolactin levels as much as 100-fold in both lactating and diestrous female rats. In contrst, 2.5 ug beta-endorphin was required in order to consistently and significantly increase circulating levels of GH by 2- to 3-fold. WIN 44,441-3 antagonized the stimulatory effects of beta endorphin on both prolactin and GH secretion. Naloxonazine pretreatment abolished the morphine-induced prolactin secretory response, without affecting the GH increase in diestrous females. In addition, it attenuated the GH secretory response but did not totally abolish it. These data indicate that beta-endorphin elicits an increase in prolactin release through an opioid specific receptor which appears to be the mu1 opioid receptor subtype. They further suggest that beta-endorphin may increase GH levels, at least partially, via its action at this mu1 site.