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UTP evokes noradrenaline release from rat sympathetic neurons by activation of protein kinase C
Author(s) -
Vartian Nina,
Moskvina Eugenia,
Scholze Thomas,
Unterberger Ursula,
Allgaier Clemens,
Boehm Stefan
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00290.x
Subject(s) - protein kinase c , protein kinase a , endocrinology , medicine , phorbol , tetrodotoxin , receptor , protein kinase inhibitor , ionomycin , biology , superior cervical ganglion , kinase , chemistry , microbiology and biotechnology , stimulation
The pathway involved in UTP‐evoked noradrenaline release was investigated in cultures of rat superior cervical ganglia. Northern blots revealed an age‐related increase in levels of mRNA for P2Y6 receptors in cultures obtained at postnatal days 1 and 5, respectively, but no change in transcripts for P2Y1 and P2Y2. Likewise, UTP‐evoked overflow of previously incorporated [ 3 H]noradrenaline was six‐fold higher in neurons obtained at postanatal day 5. Various protein kinase C inhibitors diminished UTP‐, but not electrically, induced tritium overflow by > 70%, as did down‐regulation of protein kinase C by 24 h exposure to phorbol ester. β‐Phorbol‐12,13‐dibutyrate and dioctanoylglycerol caused concentration‐dependent increases in [ 3 H] outflow of up to 6% of total radioactivity, and the secretagogue actions of these agents were reduced in the presence of protein kinase C inhibitors and in neurons pretreated with phorbol ester. Overflow evoked by dioctanoylglycerol was attenuated in the absence of extracellular Ca 2+ and in the presence of tetrodotoxin or Cd 2+ . In addition to triggering tritium overflow, UTP reduced currents through muscarinic K + channels which, however, were not affected by phorbol esters. This action of UTP was not altered by protein kinase C inhibitors. These results indicate that P2Y6 receptors mediate UTP‐evoked noradrenaline release from rat sympathetic neurons via activation of protein kinase C, but not inhibition of K M channels.