ici-154129 and naloxazone

Open field behavior was observed in conjunction with mating behavior to discern whether the effect of intraventricular (ICV) beta-endorphin (beta-END) on sexual behavior may be secondary to akinesia. Three groups of ovariectomized, estrogen-progesterone-primed rats each received counterbalanced treatments of saline ICV, 2 micrograms beta-END ICV, or 2 micrograms beta-END ICV in combination with a selective opioid receptor antagonist. Receptive behavior (lordosis) and proceptive behaviors (presentation and ear wiggling) were consistently suppressed by beta-END, while ambulation was unaffected. Rearing and grooming were generally decreased, although this effect was statistically significant in only one experiment. Pretreatment with the mu-1 antagonist naloxazone (50 mg/kg intravenously) reversed the effects of beta-END on all behaviors tested. The delta receptor antagonist ICI-154,129 (12.5 and 50 micrograms ICV) only partially reversed the sexual effects of beta-END but completely reversed the open field effects. It is concluded that the suppressive effect of beta-END on sexual behavior, while not behaviorally specific, is not secondary to opioid-induced akinesia.

Topics: Animals; Behavior, Animal; beta-Endorphin; Endorphins; Enkephalin, Leucine; Estrogens; Female; Naloxone; Narcotic Antagonists; Ovariectomy; Progesterone; Rats; Rats, Inbred Strains; Receptors, Opioid; Sexual Behavior, Animal

Administration of opioid receptor antagonists was utilized to determine the opioid receptor type involved in the suppression of LH release by beta-endorphin (beta-END). Long-term (three to four weeks) ovariectomized rats with chronic third ventricular cannulae were fitted with jugular catheters and received treatment with vehicle or one of three opioid antagonists. The delta antagonist ICI 154, 129, but not the mu1 or mu antagonists naloxazone or beta-funaltrexamine, respectively, blocked the suppressive effect of beta-END on plasma LH levels and transiently but significantly increased LH levels above preinfusion value. None of the antagonists significantly reduced the beta-END-induced release of PRL. These results provide evidence that the inhibitory effect of beta-END on LH release may be mediated by delta receptors.

Topics: Animals; beta-Endorphin; Castration; Endorphins; Enkephalin, Leucine; Female; Kinetics; Luteinizing Hormone; Naloxone; Naltrexone; Narcotic Antagonists; Prolactin; Rats; Rats, Inbred Strains; Receptors, Opioid

Administration of naloxazone (50 mg/kg i.v.), an irreversible, selective and long acting antagonist of the mu 1 subclass of the opioid receptors, strongly reduced stimulation of PRL secretion by morphine (5.0 mg/kg i.v.) injected 24 hours later into conscious, unrestrained rats. In contrast, the effect of morphine on PRL release was unimpaired in rats treated 24 hours beforehand with either the reversible opioid antagonist naloxone (50 mg/kg i.v.), or the vehicle for naloxazone. A complete suppression of the PRL response to morphine (3.0 mg/kg i.v.) was observed in animals given intraventricular (IVT) injection of beta- funaltrexamine (beta-FNA, 2.5 micrograms), another selective, irreversible and long acting antagonist of the mu receptors, 24 hours beforehand. Neither naloxazone nor beta-FNA had any effect on the activation of GH secretion by morphine, which, however, was conspicuously reduced by ICI 154, 129, a preferential delta receptor antagonist, injected IVT (50 micrograms) 5 minutes before morphine. ICI 154, 129 had no effect on the PRL response to morphine. It is concluded that the PRL stimulating effect of morphine is mediated by the mu receptors, whereas activation of GH probably involves the delta sites.

Topics: Animals; Drug Interactions; Enkephalin, Leucine; Growth Hormone; Injections, Intraventricular; Male; Morphine; Naloxone; Naltrexone; Prolactin; Rats; Rats, Inbred Strains; Receptors, Opioid