Nordmann J J, Stuenkel E L, Malviya A N
Centre de Neurochimie du CNRS, Strasbourg, France.
Biochem J. 1991 Jan 15;273(Pt 2)(Pt 2):493-6. doi: 10.1042/bj2730493.
Protein kinase C (PKC) has been implicated in the mechanism of exocytosis, although various studies have been unable to pinpoint actual translocation or activation of PKC during exocytosis. We have studied, in neurohypophysial nerve endings, intracellular Ca2+ levels, secretion of neuropeptides and PKC translocation. Neurohormone secretion was triggered by K(+)-induced or electrically induced depolarization in both the absence and the presence of phorbol esters. PKC was translocated from the cytosol to the membrane on electrical stimulation or K+ depolarization, but not to the extent obtained with phorbol ester. Data are presented clearly demonstrating that the translocation of PKC from cytosol to membrane is not required for exocytosis, nor does it alter in any way neuropeptide release from neurohypophysial nerve terminals.
蛋白激酶C(PKC)与胞吐作用机制有关,尽管各种研究都未能确定胞吐过程中PKC的实际转位或激活情况。我们研究了神经垂体神经末梢的细胞内钙离子水平、神经肽分泌和PKC转位。在不存在和存在佛波酯的情况下,钾离子诱导或电诱导的去极化均可触发神经激素分泌。电刺激或钾离子去极化时,PKC从细胞质转位至细胞膜,但转位程度不及佛波酯处理时。所呈现的数据清楚地表明,PKC从细胞质到细胞膜的转位对于胞吐作用并非必需,也不会以任何方式改变神经垂体神经末梢的神经肽释放。