To address the issue of whether, after morphine treatment, the reduced release of dopamine (DA) into portal blood is entirely responsible for the increased prolactin (PRL) release, the following study was conducted. The concentration of DA in plasma from a single portal vessel of untreated, ovariectomized rats was 1.85 ± 0.33 ng/ml (mean ± SE). Treatment of ovariectomized rats with α-methyl-p-tyrosine (αMT) caused a 91% reduction in the concentration of DA in portal plasma. Infusion of DA (0.4 μg/min/kg BW) into a jugular vein of rats pretreated with αMT restored the DA concentration in portal plasma to that seen in untreated rats. Injection of morphine sulfate elicited a marked increase in the concentration of PRL in plasma. Infusion of DA at rates of 0.4 and 0.8 μg/min/kg BW suppressed by 52 and 75%, respectively, the secretion of PRL after morphine treatment. Infusion of DA had no effect on the release of PRL induced by intra- cerebroventricularly administered β-endorphin. Although treatment of rats with αMT caused release of PRL that was similar to that seen in rats treated with morphine, infusions of DA at 0.4 and 0.8 μg/min/kg BW into αMT-treated, ovariectomized rats suppressed the secretion of PRL by 89 and 96%, respectively. Thus, after morphine treatment, the decreased release of DA into portal blood is not in itself sufficient to account for the increase seen in the secretion of PRL. It is suggested that morphine and opiate-like peptides induce the release of a hypothalamic substance(s) that stimulates PRL release.
- Prolactin releasing factor
- Tuberoinfundibular neurons
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrine and Autonomic Systems
- Cellular and Molecular Neuroscience