The Effects of Dopamine on the Release of Immunoreactive β-Endorphine-Like Peptide from the Dispersed Cells of the Rat Neurointermediate Lobe

  • FURUKI Yoshihiro
    Department of Obstetrics and Gynecology, Kumamoto University Medical School
  • MUNEMURA Masahide
    Department of Obstetrics and Gynecology, Kumamoto University Medical School
  • SAKODA Yoshio
    Department of Obstetrics and Gynecology, Kumamoto University Medical School
  • HATADA Yasuyuki
    Department of Obstetrics and Gynecology, Kumamoto University Medical School
  • MAEYAMA Masao
    Department of Obstetrics and Gynecology, Kumamoto University Medical School
  • MATSUMURA Mitsuhiro
    Department of Internal Medicine, Tokushima University Medical School

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Other Title
  • β-エンドルフィン分泌に対するドーパミンの効果-下垂体中葉遊離細胞における検討-

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The intermediate lobe of the rat pituitary gland is a homogeneous population of cells which synthesize and secrete various peptides related to ACTH and lipotropin derived from a common precursor, proopiomelanocortin. Catecholamine β-receptor (β-adrenoceptor) and dopamine receptor which are present in the intact cells of the intermediate lobe, remain functional in the enzymatically dispersed cells.<BR>In this study we investigated the mechanism by which β-endorphin is released from the dispersed cells of the neurointermediate lobe of the rat pituitary gland. 1-Isoproterenol stimulated the release of immunoreactive β-endorphin-like peptide (IR-β-Ep) and the accumulation of adenosine 3′,5′-monophosphate (cAMP). On the other hand, dopaminergic drugs, apomorphine, bromocriptine, dopamine, lergotrile and lisuride, decreased the rate of release of IR-β-Ep. Dopamine also inhibited the stimulatory effects of 1-isoproterenol on the release of IR-β-Ep and cAMP accumulation. Dopamine antagonists, fluphenazine and sulpiride, diminished the inhibitory effects of dopamine on the release of IR-β-Ep and cAMP accumulation which were stimulated by l-isoproterenol.<BR>it has been reported that cholera toxin enhanced the release of IR-β-Ep and the accumulation of cAMP in the rat neurointermediate lobe. After preincubation in the incubation medium containing 30 nM cholera toxin for 2 hours, the cells (CT cells) showed spontaneous release of IR-β-Ep and cAMP accumulation. 1-Isoproterenol had no effect on the release of IR-β-Ep and cAMP accumulation in CT cells. Dopamine, however, inhibited both the release of IR-β-Ep from CT cells and cAMP accumulation in CT cells.<BR>These results suggest that dopamine may be involved in the regulatory mechanism of IR-β-Ep release from the dispersed cells of the rat neurointermediate lobe.

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