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Titolo:
MECHANISM FOR MODULATION OF NICOTINIC ACETYLCHOLINE-RECEPTORS THAT CAN INFLUENCE SYNAPTIC TRANSMISSION
Autore:
AMADOR M; DANI JA;
Indirizzi:
BAYLOR COLL MED,DIV NEUROSCI,1 BAYLOR PLAZA HOUSTON TX 77030 BAYLOR COLL MED,DIV NEUROSCI HOUSTON TX 77030
Titolo Testata:
The Journal of neuroscience
fascicolo: 6, volume: 15, anno: 1995,
pagine: 4525 - 4532
SICI:
0270-6474(1995)15:6<4525:MFMONA>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE ACTIVITY; LONG-TERM POTENTIATION; RAT CENTRAL NEURONS; CALCIUM PERMEABILITY; EXTRACELLULAR CALCIUM; HIPPOCAMPAL SLICES; POTASSIUM CHANGES; GANGLION NEURONS; CHANNEL; SECRETION;
Keywords:
SYNAPTIC MODULATION; CALCIUM; CALCIUM MODULATION; CHOLINERGIC; NEURONAL ACH RECEPTORS; NICOTINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Physical, Chemical & Earth Sciences
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
M. Amador e J.A. Dani, "MECHANISM FOR MODULATION OF NICOTINIC ACETYLCHOLINE-RECEPTORS THAT CAN INFLUENCE SYNAPTIC TRANSMISSION", The Journal of neuroscience, 15(6), 1995, pp. 4525-4532

Abstract

Only recently has it been appreciated that neuronal nicotinic ACh receptors (NnAChRs) are highly permeable to Ca2+ and are modulated by Ca2 in a dose-dependent manner, These findings suggest that Ca2+ could have roles in cholinergic synaptic plasticity, We report a possible mechanism for Ca2+-initiated synaptic plasticity that differs from the intracellular Ca2+ cascade associated with plasticity of glutamatergic synapses, Rapid changes in external Ca2+ modulate cholinergic spontaneous synaptic currents in superior cervical ganglionic sympathetic neurons, Inhibition of cholinergic currents by chlorisondamine, which blocks only open channels and becomes trapped in the pore, showed that the modulation is not by a mechanism that activates a previously unresponsive population of NnAChRs, Rather, single-channel recordings with ganglionic NnAChRs from chromaffin cells indicated that Ca2+ directly alters the probability of the channels being open, We hypothesize from theresults that activity-dependent decreases in external Ca2+, which occur throughout the nervous system, could directly underlie a rapid negative-feedback mechanism that decreases the responsiveness of NnAChRs at synapses, When external Ca2+ is decreased, presynaptic Ca2+ currentsand transmitter release also are diminished, Thus, several mechanismscould combine to potently and rapidly depress synaptic nicotinic receptors until the external Ca2+ concentration recovers.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 11:16:17