Stimulation of prolactin secretion in the rat by α-neo-endorphin, β-neo-endorphin and dynorphin

Matsushita, Norio; Kato, Yuzuru; Shimatsu, Akira; Katakami, Hideki; Fujino, Masahiko; Matsuo, Hisayuki; Imura, Hiroo

doi:10.1016/0006-291x(82)91552-2

Cited by 27 publications

(13 citation statements)

References 12 publications

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“…The majority of the studies points to a lack of effect of B-EP at the anterior pituitary to directly stimulate PRL release [14,17,24,29,30] or reverse the do paminergic inhibition of PRL [24], However, studies re ported by Lien et al [23] showed a direct stimulatory effect of met-and leu-enkephalins on PRL release from monolayer cultures of rat anterior pituitary cells. Consistent with these findings are the demonstrations by Matsushita et al [25] that PRL release from perfused pituitary cells in vitro can be stimulated by a-neo-endorphin in a dose-dependent manner. Furthermore, Enjalbert et al [14] reported that B-EP, morphine and met-enkephalin can suppress the inhibi tory effect of dopamine on PRL release from rat anterior pituitaries incubated in vitro, and the effects can be antag onized by naloxone.…”

supporting

confidence: 79%

“…However, due to the transient nature of the effect, and the high con centration of B-EP required to elicit a response of small magnitude, the B-EP effect may be merely a pharmacologic phenomenon, and may have little physiologic significanes. The ineffectiveness of B-EP in stimulating basal PRL re lease is different from that reported by Lien et al [23] where enkephalins at concentrations as low as 5 ng/ml were shown to stimulate basal PRL release in a 3-hour incuba tion experiment, and by Matsushita et al [25] where a-neoendorphin from 10" to 10" M was shown to stimulate PRL release in a cell perfusion system.…”

Section: Discussioncontrasting

confidence: 53%

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Does β-Endorphin Modulate Basal and Dopamine-Inhibited Prolactin Release by an Action at the Anterior Pituitary?

Cheung¹

1984

Neuroendocrinology

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Previous studies performed to elucidate an anterior pituitary site of action for β-endorphin (B-EP) in the regulation of prolactin (PRL) release have been inconclusive. The purpose of the present study was to further investigate if B-EP could stimulate PRL release by a direct action at the anterior pituitary. Anterior pituitaries from ovariectomized rats were dispersed, and the cells were plated in Ham’s F-10 medium. Following a 48-hour preincubation period, the effects of B-EP on basal PRL release and on the dopamine-inhibited PRL release were studied over a 24-hour period. Overall, B-EP at concentrations ranging from 10^–8 to 10^–6 M had no effect on basal release of PRL at 1, 3, 5 and 24 h, although a small but significant increase of 39% was observed with 10^–6 M B-EP at 1 h of incubation only. B-EP at 10^–6 M, but not at lower concentrations, significantly suppressed the inhibitory effects of 10^–6 M dopamine on PRL release at 1 h but not at longer periods of incubation. Pretreatment of the cells for 3 h with 10^–6 M naloxone completely antagonized the suppressive effect of B-EP on the dopamine-mediated inhibition of PRL release. Naloxone pretreatment of the cells had no effect on basal nor dopamine-inhibited release of PRL. Because of the high concentration of B-EP required to suppress the dopamine inhibition and the transitory nature of this B-EP effect, it is unlikely that the primary site of action for B-EP in regulating PRL release is at the anterior pituitary. However, high concentrations of B-EP may antagonize the inhibitory effect of dopamine on PRL release at the anterior pituitary through a specific opiate-mediated mechanism.

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supporting

confidence: 79%

Section: Discussioncontrasting

confidence: 53%

Does β-Endorphin Modulate Basal and Dopamine-Inhibited Prolactin Release by an Action at the Anterior Pituitary?

Cheung¹

1984

Neuroendocrinology

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“…dynorphin-A(l-l3) kept PRL levels signifi cantly elevated for a duration longer than that produced by dynorphin-A(i-IO)-amide. The effects of dynorphin-A on plasma PRL concentrations observed in these studies agree with previous rat studies in which naloxone-reversible plasma PRL increases were observed after intraventricular injections of dynorphin-A( I -13) [12]. Additional studies are needed to determine the precise site of dynorphin-A action on PRL secretion.…”

Section: Discussionsupporting

confidence: 81%

Consequence of Dynorphin-A Administration on Anterior Pituitary Hormone Concentrations in the Adult Male Rhesus Monkey

1987

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This study examines the role of dynorphin-A(1-13) and dynorphin-A(1-10)-amide in the neuroendocrine regulation of anterior pituitary hormones in nonrestrained, adult male rhesus monkeys. The effects of these opioids on plasma concentrations of prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyrotropin (TSH) and growth hormone (GH) were assessed. Intravenous administration of dynorphin-A(1–13), 1–120 µg/kg, significantly increased plasma PRL levels. Average maximal increases of 90–230% occurred within 5 min and levels remained significantly elevated for up to 120 min. PRL response reached a plateau following the 30 µg/kg dose. Dynorphin-A(1–13) had no observable effects on plasma concentrations of LH, FSH, TSH or GH at any dose level studied. Administration of dynorphin-A(1–10)-amide produced significant dose-dependent increases in plasma PRL concentrations. Dose levels of 1–120 µg/kg produced mean peak increases from 100 to 230%, 5–10 min postadministration. Dynorphin-A(1–10)-amide had no significant effect on plasma concentrations of LH, FSH, TSH or GH. The increases in plasma PRL concentrations induced by dynorphin-A were naloxone-reversible. These results indicate a selective effect of dynorphin-A on the regulatory mechanisms of PRL secretion over that of other anterior pituitary hormones.

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“…It is presently believed that the opioids modify prolactin release through a central nervous sys¬ tem mechanism (Rivier et al, 1977;Matsushita et al, 1982;Giudici et al, 1984), which involves the activation of specific brain receptors of the mu and kappa families (Spiegel, Kouzides & Pasternak, 1982;Koenig & Krulich, 1984). The loss of effectiveness of morphine on prolactin secretion induced by orchidectomy may therefore be due to an alteration, induced by castration, of the number or of the binding characteristics of brain mu and kappa receptors.…”

Section: Resultsmentioning

confidence: 99%

“…(Rivier et al, 1977;Chihara et al, 1978;Kato et al, 1978Kato et al, ,1982Panerai et al, 1981;Van Vugt et al, 1981;Matsushita et al, 1982;Giudici etal, 1984). The experiments performed in long-term castrated rats clearly show that even the i.v.t.…”

Section: Introductionmentioning

confidence: 99%

Morphine stimulates prolactin release in normal but not in castrated male rats

Limonta¹,

Piva²,

Maggi³

et al. 1986

Reproduction

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Stimulation of prolactin secretion in the rat by α-neo-endorphin, β-neo-endorphin and dynorphin

Cited by 27 publications

References 12 publications

Does β-Endorphin Modulate Basal and Dopamine-Inhibited Prolactin Release by an Action at the Anterior Pituitary?

Does β-Endorphin Modulate Basal and Dopamine-Inhibited Prolactin Release by an Action at the Anterior Pituitary?

Consequence of Dynorphin-A Administration on Anterior Pituitary Hormone Concentrations in the Adult Male Rhesus Monkey

Morphine stimulates prolactin release in normal but not in castrated male rats

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