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Titolo:
Ca2+-induced Ca2+ release activates spontaneous miniature outward currents(SMOCs) in parasympathetic cardiac neurons
Autore:
Merriam, LA; Scornik, FS; Parsons, RL;
Indirizzi:
Univ Vermont, Coll Med, Dept Anat & Neurobiol, Burlington, VT 05405 USA Univ Vermont Burlington VT USA 05405 Neurobiol, Burlington, VT 05405 USA
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 2, volume: 82, anno: 1999,
pagine: 540 - 550
SICI:
0022-3077(199908)82:2<540:CCRASM>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED CALCIUM-RELEASE; BULLFROG SYMPATHETIC NEURONS; CA2+-ACTIVATED K+ CHANNELS; VAGAL AFFERENT NEURONS; ROOT GANGLION-CELLS; SARCOPLASMIC-RETICULUM; RYANODINE RECEPTOR; ENDOGENOUS EFFECTORS; SMOOTH-MUSCLE; CAFFEINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Parsons, RL Univ Vermont, Coll Med, Dept Anat & Neurobiol, Burlington, VT 05405 USA Univ Vermont Burlington VT USA 05405 Burlington, VT 05405 USA
Citazione:
L.A. Merriam et al., "Ca2+-induced Ca2+ release activates spontaneous miniature outward currents(SMOCs) in parasympathetic cardiac neurons", J NEUROPHYS, 82(2), 1999, pp. 540-550

Abstract

Mudpuppy parasympathetic cardiac neurons exhibit spontaneous miniature outward currents (SMOCs) that are thought to be due to the activation of clusters of large conductance Ca2+-activated K+ channels (BK channels) by localized release of Ca2+ from internal stores close to the plasma membrane. Perforated-patch whole cell recordings were used to determine whether Ca2+ induced Ca2+ release (CICR) is involved in SMOC generation. We confirmed that BK channels are involved by showing that SMOCs are inhibited by 100 nM iberiotoxin or 500 mu M tetraethylammonium (TEA), but not by 100 nM apamin. SMOGfrequency is decreased in solutions that contain 0 Ca2+/3.6 mM Mg2+, and also in the presence of 1 mu M nifedipine and 3 mu M omega-conotoxin GVIA, suggesting that SMOG activation is dependent on calcium influx. However, Ca2 influx alone is not sufficient; SMOG activation is also dependent on Ca2release from the caffeine- and ryanodine-sensitive Ca2+ store, because exposure to 2 mM caffeine consistently caused an increase in SMOG frequency, and 10-100 mu M ryanodine altered the configuration of SMOCs and eventually inhibited SMOG activity. Depletion of intracellular Ca2+ stores by the Ca-ATPase inhibitor cyclopiazonic acid (10 mu M) inhibited SMOG activity, even when Ca2+ influx was not compromised. We also tested the effects of the membrane-permeable Ca2+ chelators, bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid-AM (BAPTA-AM) and EGTA-AM. EGTA-AM (10 mu M) caused no inhibition of SMOG activation, whereas 10 mu M BAPTA-AM consistently inhibited SMOCs. After SMOCs were completely inhibited by BAPTA, 3 mM caffeine caused SMOG activity to resume. This effect was reversible on removal of caffeine and suggests that the source of Ca2+ that triggers the internal Ca2+ release channel is different from the source of Ca2+ that activates clusters of BK channels. We propose that influx of Ca2+ through voltage-dependent Ca2+ channels isrequired for SMOG generation, but that the influx of Ca2+ triggers CICR from intracellular stores, which then activates the BK channels responsible for SMOG generation.

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Documento generato il 25/11/20 alle ore 18:55:05