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Tonic inhibition and rebound facilitation of a neuronal calcium channel by a GTP-binding protein.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kasai, H.
Description	Author Affiliation: Kasai H ( Abteilung Membranbiophysik, Max-Planck-Institut für Biophysikalische Chemie, Göttingen, Federal Republic of Germany.);
Abstract	A significant fraction of differentiated NG108-15 neuroblastoma/glioma cells have Ca2+ channel current different from that of undifferentiated cells. In the former cells, the Ca2+ channel sensitive to omega-conotoxin GVIA had slowed activation kinetics and was facilitated by depolarizing prepulses. These kinetic features are identical to those produced by inhibition of the channel by G proteins. Prolonged treatment with prostaglandin E1 and theophylline, agents that cause cellular differentiation, promoted incidence and extent of the tonic inhibition. Intracellular guanosine 5'-[beta-thio]diphosphate removed the tonic inhibition, suggesting sustained activation of a G protein, but pertussis toxin did not block it. A sulfhydryl alkylating agent, N-ethylmaleimide (0.1 mM), rapidly eliminated agonist-induced inhibition, whereas N-ethylmaleimide spared the tonic inhibition and the one induced by intracellular guanosine 5'-[gamma-thio]triphosphate. An agonist could further inhibit the Ca2+ channel that was already tonically inhibited. After washout of an inhibitory agonist, the tonic inhibition was temporarily removed. This 'rebound facilitation' gradually faded within a few minutes. Pertussis toxin or N-ethylmaleimide prevented the rebound facilitation, whereas phorbol ester, forskolin, or arachidonic acid induced neither the rebound facilitation nor the tonic inhibition. Whatever its mechanism, the tonic inhibition of Ca2+ channels may serve as the basis for long-term and bidirectional regulation of activity of neuronal Ca2+ channels.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	19
Volume Number	88
Language	English
Publisher	National Academy of Sciences
Publisher Date	1991-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Calcium Channels Physiology GTP-Binding Proteins Neurons Animals Drug Effects Enkephalin, D-Penicillamine (2,5)- Enkephalins Pharmacology Ethylmaleimide In Vitro Techniques Membrane Potentials Mollusk Venoms Neuroblastoma Peptides, Cyclic Pertussis Toxin Tumor Cells, Cultured Virulence Factors, Bordetella Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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