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Titolo:
ROLE OF CA2+ IONS IN NICOTINIC FACILITATION OF GABA RELEASE IN MOUSE THALAMUS
Autore:
LENA C; CHANGEUX JP;
Indirizzi:
INST PASTEUR,CTR NATL RECH SCI,URA D1284,25 RUE DR ROUX F-75724 PARIS15 FRANCE INST PASTEUR,CTR NATL RECH SCI,URA D1284 F-75724 PARIS 15 FRANCE
Titolo Testata:
The Journal of neuroscience
fascicolo: 2, volume: 17, anno: 1997,
pagine: 576 - 585
SICI:
0270-6474(1997)17:2<576:ROCIIN>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
LATERAL GENICULATE-NUCLEUS; EXCITATORY SYNAPTIC TRANSMISSION; FROG NEUROMUSCULAR-JUNCTION; ADRENAL CHROMAFFIN CELLS; SUBUNIT MESSENGER-RNAS; OPTIC-NERVE TERMINALS; RAT CENTRAL NEURONS; ACETYLCHOLINE-RECEPTORS; INTERPEDUNCULAR NUCLEUS; CHOLINERGIC RECEPTORS;
Keywords:
NICOTINIC ACETYLCHOLINE RECEPTORS; PRESYNAPTIC; FACILITATION; GABA; CALCIUM; THALAMUS (SENSORY NUCLEI);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
65
Recensione:
Indirizzi per estratti:
Citazione:
C. Lena e J.P. Changeux, "ROLE OF CA2+ IONS IN NICOTINIC FACILITATION OF GABA RELEASE IN MOUSE THALAMUS", The Journal of neuroscience, 17(2), 1997, pp. 576-585

Abstract

Presynaptic nicotinic acetylcholine receptors (nAChRs) are present inmany regions of the brain and potentially serve as targets for the pharmacological action of nicotine in vivo. To investigate their mechanism of action, we performed patch-clamp recordings in relay neurons from slices of thalamus sensory nuclei. In these nuclei, nAChR activationfacilitated the release of the inhibitory neurotransmitter GABA. Micromolar concentrations of nicotinic agonists increased the frequency ofminiature GABAergic synaptic currents and decreased the failure rate of evoked synaptic currents. These actions of nicotinic agonists were not observed in knock-out mice lacking the beta 2 nAChR subunit gene. Nicotinic effects were dependent on extracellular calcium ions, and they persisted when calcium was replaced by strontium or barium but not by magnesium. Furthermore, in high extracellular calcium concentrations, nicotinic agonists evoked an increase in spontaneous release lasting for minutes after removal of the agonist. This supports the view that presynaptic nAChRs facilitate the release of neurotransmitter by increasing the calcium concentrations in presynaptic nerve endings. With use of cadmium and nickel ions as selective blockers, it was found that in different sensory nuclei the presynaptic influx of calcium could result either from the activation of voltage-dependent calcium channels or from a direct influx through nAChR channels. Finally, we propose that the nicotinic facilitation of GABAergic transmission may contribute to the increase of signal-to-noise ratio observed in the thalamus in vivo during arousal.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 22:26:16