Callahan P, Janik J, Grandison L, Rabii J
Department of Biological Sciences, Rutgers University, Piscataway, NJ 08855.
Brain Res. 1988 Mar 1;442(2):214-22. doi: 10.1016/0006-8993(88)91506-5.
The ability of morphine to stimulate prolactin and growth hormone (GH) release was investigated in male rats and in female rats during diestrus, proestrus and lactation. In agreement with previous reports, acute morphine administration produced an increase in circulating levels of prolactin in male and in diestrous and proestrous female rats. In contrast to these results, morphine administration (10 or 15 mg/kg, s.c.; 5 mg/kg, i.v.; 5 or 10 micrograms, i.c.v.) did not produce an increase in prolactin levels in lactating dams. Morphine stimulates prolactin release in part by decreasing dopamine turnover in the tuberoinfundibular neurons in the median eminence. In order to assess the functional activity of these neurons during lactation, haloperidol (0.1 or 0.5 mg/kg, i.v.) was given to lactating dams. There was a significant increase in prolactin levels following haloperidol administration, suggesting that these dopaminergic neurons are participating in the modulation of prolactin release during lactation. In contrast to the insensitivity of the lactating rat to morphine stimulation of prolactin release, the intraventricular administration of two other opiate receptor agonists, beta-endorphin (10 or 20 micrograms) and [D-Ala-D-Leu]enkephalin (DADLE; 5 or 10 micrograms), produced significant increases in circulating levels of this hormone. The GH response to morphine, beta-endorphin and DADLE was also measured in these same rats. All these opiate receptor agonists stimulated GH release in male rats and in female rats during diestrus and proestrus as well as during lactation. These observations suggest that the suckling stimulus during lactation renders the rat refractory to morphine stimulation of prolactin release, possibly as a result of down-regulation of the mu-opiate receptor subtype.
