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Titolo:
Muscarinic receptors mediate enhancement of spontaneous GABA release in the chick brain
Autore:
Guo, JZ; Chiappinelli, VA;
Indirizzi:
George Washington Univ, Sch Med & Hlth Sci, Dept Pharmacol, Washington, DC20037 USA George Washington Univ Washington DC USA 20037 l, Washington, DC20037 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 95, anno: 2000,
pagine: 273 - 282
SICI:
0306-4522(2000)95:1<273:MRMEOS>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
LATERAL SPIRIFORM NUCLEUS; IN-VIVO MICRODIALYSIS; ACETYLCHOLINE-RECEPTORS; NICOTINIC RECEPTORS; SYNAPTIC TRANSMISSION; PREFRONTAL CORTEX; ADENYLYL CYCLASE; CALCIUM CHANNELS; DOPAMINE RELEASE; RAT HIPPOCAMPUS;
Keywords:
muscarinic receptors; nicotinic receptors; presynaptic; pre-terminals; modulation of GABA release; lateral spiriform nucleus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Guo, JZ George Washington Univ, Sch Med & Hlth Sci, Dept Pharmacol, Washington, DC20037 USA George Washington Univ Washington DC USA 20037 ngton, DC20037 USA
Citazione:
J.Z. Guo e V.A. Chiappinelli, "Muscarinic receptors mediate enhancement of spontaneous GABA release in the chick brain", NEUROSCIENC, 95(1), 2000, pp. 273-282

Abstract

The functional role of muscarinic acetylcholine receptors in the lateral spiriform nucleus was studied in chick brain slices. Whole-cell patch-clamp recordings of neurons in the lateral spiriform nucleus revealed that carbachol enhanced GABAergic spontaneous inhibitory postsynaptic currents. The duration of the response to carbachol was significantly reduced after blockade of muscarinic receptors with atropine. In the presence of the nicotinic receptor antagonist dihydro-beta-erythroidine, carbachol produced a delayed but prolonged enhancement of spontaneous GABAergic inhibitory postsynaptic currents that was completely blocked by atropine. Muscarine also enhanced the frequency of spontaneous GABAergic inhibitory postsynaptic currents in adose-dependent manner, but had no effect on inhibitory postsynaptic current amplitude. While 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride, a M-3 antagonist, completely blocked muscarine's effect, telenzepine,a M-1 antagonist, and tropicamide, a M-4 antagonist, only partially decreased the response to muscarine. Pirenzepine, a M-1 antagonist, and methoctramine, a M-2 antagonist, potentiated muscarine's enhancement of spontaneous GABAergic inhibitory postsynaptic currents. Muscarine's action was blocked by tetrodotoxin, cadmium chloride and omega-conotoxin GVIA, but was not affected by dihydro-beta-erythroidine, 6-cyano-7-nitroquinoxaline-2.3-dione, D(-)-2-amino-5-phosphonopentanoic acid, naloxone or fluphenazine. These results demonstrate that activation of both muscarinic and nicotinicacetylcholine receptors can enhance GABAergic inhibitory postsynaptic currents in the lateral spiriform nucleus. The muscarinic response has a sloweronset but lasts longer than the nicotinic effect. The M-3 receptor subtypeis predominantly involved in enhancing spontaneous GABAergic inhibitory postsynaptic currents. These M-3 receptors must be located some distance fromGABA release sites, since activation of voltage-dependent sodium channels,and consequent activation of N-type voltage-dependent calcium channels, isrequired to trigger enhanced GABA release following activation of muscarinic receptors. (C) 1999 IBRO. Published by Elsevier Science Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/12/20 alle ore 21:30:20