Relationship between Dopamine Release into Hypophysial Portal Blood and Prolactin Release after Morphine Treatment in Rats

Abstract

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.

Sex Difference in κ-Opioid Receptor (KOPR)-Mediated Behaviors, Brain Region KOPR Level and KOPR-Mediated Guanosine 5′-O-(3-[35S]Thiotriphosphate) Binding in the Guinea Pig

“…It has to be noted, however, that the expression of KOPR is only one of several mechanisms. Indeed, tuberoinfundibular dopaminergic neuronal activity and prolactin-releasing factors are also important factors (Arita and Porter, 1984;Shin et al, 1988).…”

Involvement of Endogenous Opioidergic Neurons in Modulation of Prolactin Secretion in Response to Mating in the Female Rat

“…Treatment of NAL during the nocturnal surge in pregnant rats suppresses PRL secretion, whereas dihydroxyphenylalanine (DOPA) accumulation in the stalk median eminence [11]and FRA expression in TIDA neurons significantly increase [48]. However, Arita and Porter [49]demonstrated that the dopamine mechanism is insufficient to account for all the EOP-induced PRL release. Indeed, intraventricular administration of β-END antiserum blocks sucking-induced PRL release without affecting TIDA neuronal activity [36].…”

Suckling-Induced Prolactin Release is Suppressed by Naloxone and Simulated by β-Endorphin

“…These results are consis tent with the suggestion that opiate neurons are situated in the neuronal pathway mediating this neuroendocrine reflex response. In response to the suckling stimulus, opiate neu rons could be inhibitory to tuberoinfundibular dopaminer gic (TIDA) neurons [7,35] and/or stimulatory to PRL-releasing factor (PRF) neurons [2] depending upon the exact nature of the neural mechanism mediating suckling-in duced PRL release. Alternatively, the NAL data are con sistent with the possibility that opiate neurons are not situ ated in the suckling pathway but are located such that they can modulate neuronal transmission in this pathway.…”