Voltage-dependent potentiation of neuronal l-type calcium channels
due to state-dependent phosphorylation.
Sculptoreanu, Adrian, Alexandre Figourov, and William C. De Groat.
W. C. de Groat, Department of Pharmacology, University of
Pittsburgh, Pittsburgh, PA 15261, Figourov and A. Sculptoreanu, Lady
Davis Institute for Medical Research of Sir Mortimer B. Davis Jewish
General Hospital, Montr[acute]eal, Quebec, H3T 1E2, and Depts. of
Surgery and Experimental Medicine, Faculty of Medicine, McGill
University
APStracts 2:0164C, 1995.
Modulation of calcium channels during repetitive activity in excitable
cells can have an important role in altering cellular function. In
mammalian parasympathetic and dorsal root ganglion neurons, L-type
Ca2+ channels are potentiated by single depolarizing prepulses or
trains of short high frequency depolarizing pulses. This type of
potentiation takes place regardless whether Ca2+ or Ba2+ are the
charge carriers and requires phosphorylation by a cAMP-dependent
protein kinase. The magnitude of facilitation was correlated with
frequency of conditioning trains, was enhanced by 8Br-cAMP or Sp
-isomer and reduced by the Rp-isomer or a peptide inhibitor of cAMP
-dependent protein kinase. The N-type Ca2+ channels exhibited the
opposite response to these agents. We propose that the potentiation
of L-type Ca2+ channel currents in neurons is due to state-dependent
phosphorylation by cAMP dependent protein kinase (Sculptoreanu et al.
Nature Lond. 364: 240-243, 1993, Proc. Natl. Acad. Sci. USA 90:
10135-10139, 1993). Thus state-dependent phosphorylation in neurons
may be a mechanism for the regulation of various functions including
transmitter release.
Received 18 October 1994; accepted in final form 5 April 1995.
APS Manuscript Number C624-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.