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Titolo:
Cyclic nucleotide-gated channels contribute to the cholinergic plateau potential in hippocampal CA1 pyramidal neurons
Autore:
Kuzmiski, JB; MacVicar, BA;
Indirizzi:
Univ Calgary, Fac Med, Dept Physiol & Biophys, Neurosci Res Grp, Calgary, AB T2N 4N1, Canada Univ Calgary Calgary AB Canada T2N 4N1 s Grp, Calgary, AB T2N 4N1, Canada
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 22, volume: 21, anno: 2001,
pagine: 8707 - 8714
SICI:
0270-6474(20011115)21:22<8707:CNCCTT>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
L-CIS-DILTIAZEM; GMP-ACTIVATED CONDUCTANCE; LONG-TERM POTENTIATION; NITRIC-OXIDE SYNTHASE; GUANYLYL CYCLASE; CATION CONDUCTANCE; ROD PHOTORECEPTORS; RAT HIPPOCAMPUS; SALAMANDER RODS; CALCIUM;
Keywords:
seizure; acetylcholine; muscarinic receptors; cGMP; guanylate cyclase; hippocampus; epilepsy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: MacVicar, BA Univ Calgary, Fac Med, Dept Physiol & Biophys, Neurosci Res Grp, 3330 HospDr NW, Calgary, AB T2N 4N1, Canada Univ Calgary 3330 Hosp Dr NW Calgary AB Canada T2N 4N1 Canada
Citazione:
J.B. Kuzmiski e B.A. MacVicar, "Cyclic nucleotide-gated channels contribute to the cholinergic plateau potential in hippocampal CA1 pyramidal neurons", J NEUROSC, 21(22), 2001, pp. 8707-8714

Abstract

Plateau potentials are prolonged membrane depolarizations that are observed in hippocampal pyramidal neurons when spiking and Ca2+ entry occur in combination with muscarinic receptor activation. In this study, we used whole-cell voltage clamping to study the current underlying the plateau potentialand to determine the cellular signaling pathways contributing to this current. When combined with muscarinic stimulation, depolarizing command potentials that evoked Ca2+ influx elicited a prolonged tail current (I-tail) that had an extrapolated reversal potential of -20 mV. I-tail was not observedwhen intracellular Ca2+ levels were chelated with 10 mM intracellular BAPTA, and I-tail was reversibly depressed in low external sodium. When I-tail was evoked at intervals >3 min, current amplitudes were stable for up to 1 hr. However, at shorter intervals, I-tail was refractory, with a time constant of recovery of 43.5 sec. The inhibitors of soluble guanylate cyclase 1H-[1,2,4] oxadiazolo[4,3- a] quinoxalin-1-one and 6-anilino-5,8-quinolinequinone depressed I-tail and zaprinast, which blocks cGMP-specific phosphodiesterase, enhanced I-tail, suggesting that a component of I-tail was activated by cGMP. The inhibitors of cyclic nucleotide-gated (CNG) channels L-cis-diltiazem and 2',4'-dichlorobenzamil reversibly depressed I-tail. However, protein kinase G inhibition had no effect. Therefore, these results indicatethat a component of I-tail is attributable to activation of CNG channels. We conclude that Ca2+ influx when combined with muscarinic receptor activation activates soluble guanylate cyclase and increases cGMP levels. The increased cGMP activates CNG channels and leads to prolonged depolarization. The cation conductance of the CNG channel contributes to the prolonged depolarization of the plateau potential.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 18:24:45