mu-Opioid receptor modulates peptide release from rat neurohypophysial terminals by inhibiting Ca(2+) influx.
作者： S. I. Ortiz-Miranda , G. Dayanithi , V. Coccia , E. E. Custer , S. Alphandery
DOI: 10.1046/J.1365-2826.2003.01076.X
关键词:
摘要: The activation of opioid receptors in neurones the central nervous system leads to a variety effects including modulation diuresis and parturition, processes that are directly controlled by hypothalamic-neurohypophysial (HNS). mu-opioid receptor on peptide release, voltage-gated Ca2+ currents intracellular calcium levels ([Ca2+]i) were studied isolated nerve terminals HNS. mu-receptor agonist, DAMGO ([d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin) inhibited high K+-induced release dose-dependent manner, with oxytocin being more sensitive block than vasopressin at all concentrations tested. addition antagonist CTOP (d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr amide) was able overcome inhibitory DAMGO. By contrast previous results, blockage this inhibition also prevented CTOP. Furthermore, [Ca2+]i measurements Fura-2 corroborated entry its reversal micro -receptor these terminals. Thus, decrease neuropeptide particularly for oxytocin, induced neurohypophysial is mediated, least part, corresponding due channels.
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