Cyclic GMP and protein kinase G inhibit the quantal transmitter release induced by protein kinase C

Protein kinase G inhibits the spontaneous release of acetylcholine quanta at the frog neuromuscular junction a sshown by the effects of H-8, a G kinase blocking agent. Moreover, the permeant dibutyryl cGMP blocked the frequency increase obtained in the presence of protein kinase C activators (diacyl...

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Veröffentlicht in:	Brain research 1988-11, Vol.4 (3), p.263-266
Hauptverfasser:	Brǎnişteanu, Dimitrie D., Popescu, Laurenţiu M., Brǎnişteanu, Dumitru D., Haulicǎ, Ion D.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cyclic GMP - analogs & derivatives Dibutyryl Cyclic GMP - pharmacology Enzyme Inhibitors - pharmacology In Vitro Techniques Neuromuscular Junction - drug effects Neuromuscular Junction - physiology Protein kinase A Protein kinase C Protein Kinase C - pharmacology Protein kinase G Protein Kinases - pharmacology Quantal release Rana ridibunda Synaptic Transmission - drug effects Time Factors
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Beschreibung
Zusammenfassung:	Protein kinase G inhibits the spontaneous release of acetylcholine quanta at the frog neuromuscular junction a sshown by the effects of H-8, a G kinase blocking agent. Moreover, the permeant dibutyryl cGMP blocked the frequency increase obtained in the presence of protein kinase C activators (diacylglycerol and phorbol ester) while the cAMP activated protein kinase A did show only an additive effect.
ISSN:	0169-328X 0006-8993 1872-6941
DOI:	10.1016/0169-328X(88)90034-4