Exocytosis in neurohypophysial nerve terminals is not coupled to protein kinase C translocation.
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.
Nordmann
J J
JJ
Centre de Neurochimie du CNRS, Strasbourg, France.
Stuenkel
E L
EL
Malviya
A N
AN
D000470:Alkaloids / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport; D002451:Cell Compartmentation; D003600:Cytosol / Q000201:enzymology; D004558:Electric Stimulation; D004789:Enzyme Activation / Q000187:drug effects; D005089:Exocytosis; D009411:Nerve Endings / Q000201:enzymology / Q000378:metabolism*; D009490:Neurosecretory Systems / Q000201:enzymology / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology*; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D019311:Staurosporine; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014667:Vasopressins / Q000378:metabolism*
D000470:Alkaloids; D014667:Vasopressins; D011493:Protein Kinase C; D019311:Staurosporine; D013755:Tetradecanoylphorbol Acetate; D011188:Potassium