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Titolo:
EVIDENCE FOR INVOLVEMENT OF THE VOLTAGE-DEPENDENT NA-INDUCED ACTIVATION OF G-PROTEINS( CHANNEL GATING IN DEPOLARIZATION)
Autore:
COHENARMON M; SOKOLOVSKY M;
Indirizzi:
TEL AVIV UNIV,SACKLER SCH MED,DEPT PHYSIOL & PHARMACOL IL-69978 TEL AVIV ISRAEL TEL AVIV UNIV,GEORGE S WISE FAC LIFE SCI,DEPT BIOCHEM,NEUROBIOCHEM LAB IL-69978 TEL AVIV ISRAEL
Titolo Testata:
The Journal of biological chemistry
fascicolo: 13, volume: 268, anno: 1993,
pagine: 9824 - 9838
SICI:
0021-9258(1993)268:13<9824:EFIOTV>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUANINE-NUCLEOTIDE-BINDING; SENSITIVE SODIUM-CHANNELS; MUSCARINIC ACETYLCHOLINE-RECEPTORS; BETA-ADRENERGIC RECEPTORS; HIGH-AFFINITY BINDING; RAT-BRAIN; PERTUSSIS-TOXIN; ION CHANNELS; GTP-BINDING; PHOSPHOLIPID-VESICLES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
60
Recensione:
Indirizzi per estratti:
Citazione:
M. Cohenarmon e M. Sokolovsky, "EVIDENCE FOR INVOLVEMENT OF THE VOLTAGE-DEPENDENT NA-INDUCED ACTIVATION OF G-PROTEINS( CHANNEL GATING IN DEPOLARIZATION)", The Journal of biological chemistry, 268(13), 1993, pp. 9824-9838

Abstract

Evidence for activation of pertussis-toxin-sensitive G-proteins by membrane depolarization in rat brain-stem synaptoneurosomes was recentlyreported (Coben-Armon, M., and Sokolovsky, M. (1991) J. Biol. Chem. 266, 2595-2605; (1991) Neurosci. Lett. 126, 87-90) and is further supported in this study by the observation that the depolarization-induced effect is inhibited when G-proteins are stabilized in the non-activated state with guanosine 5'-O-(2-thiodiphosphate) (GDPbetaS), which was introduced into synaptoneurosomes during the process of permeabilization and resealing. In the present study, agents that either keep the voltage-dependent Na+ channel in persistently activated state (while Nacurrents are blocked) or prevent it from activation were used in an attempt to determine whether the voltage-dependent Na+ channels are involved in the depolarization-induced activation of pertussis-toxin-sensitive G-proteins. The main probe employed was the cardiotonic and antiarrhythmic agent DPI, which is a racemic mixture of two enantiomers, one of which (the R enantiomer) reportedly prevents depolarization-induced activation of the Na+ channel while the other (the S enantiomer) inhibits Na+ channel inactivation. The results suggest that while inactivation of the voltage-dependent Na+ channel does not interfere with the putative depolarization-induced activation of G-proteins, membrane depolarization affects G-proteins and the coupled muscarinic receptorsonly if the voltage-dependent Na+ channels are capable of being activated. Thus, inhibition of the depolarization-induced activation of Nachannels was accompanied by inhibition of the depolarization-induced activation of pertussis-toxin-sensitive G-proteins and by modifications of both the coupling of G-proteins to muscarinic receptors and the ADP-ribosylation of G(o)-proteins. These effects could be counteracted by persistent activation of the voltage-dependent Na+ channels (while Na+ current was blocked). Our observations may suggest that the voltage-dependent Na+ channel gating is involved in the depolarization-induced activation of pertussis toxin-sensitive G-proteins and may provide evidence for a possible mechanism of membrane depolarization signal transduction in excitable cells.

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Documento generato il 02/12/20 alle ore 18:15:04