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Titolo:
AMPA-evoked acetylcholine release from cultured spinal cord motoneurons and its inhibition by GABA and glycine
Autore:
Fontana, G; Taccola, G; Galante, J; Salis, S; Raiteri, M;
Indirizzi:
Univ Genoa, Dipartimento Med Sperimentale, Sezione Farmacol & Tossicol, I-16148 Genoa, Italy Univ Genoa Genoa Italy I-16148 Farmacol & Tossicol, I-16148 Genoa, Italy
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 106, anno: 2001,
pagine: 183 - 191
SICI:
0306-4522(2001)106:1<183:AARFCS>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYOTROPHIC-LATERAL-SCLEROSIS; SUBUNIT MESSENGER-RNAS; SYNAPTIC TRANSMISSION; RAT MOTONEURONS; MOTOR-NEURONS; IN-VITRO; GLUTAMATE RECEPTORS; TRANSMITTER RELEASE; KAINATE RECEPTORS; NERVE-TERMINALS;
Keywords:
ACh release; primary cultures; AMPA receptors; GABAA receptors; glycine receptors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Raiteri, M Univ Genoa, Dipartimento Med Sperimentale, Sezione Farmacol & Tossicol, Viale Cembrano 4, I-16148 Genoa, Italy Univ Genoa Viale Cembrano 4Genoa Italy I-16148 8 Genoa, Italy
Citazione:
G. Fontana et al., "AMPA-evoked acetylcholine release from cultured spinal cord motoneurons and its inhibition by GABA and glycine", NEUROSCIENC, 106(1), 2001, pp. 183-191

Abstract

The release of [H-3]acetylcholine evoked by alpha -amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) and its inhibition mediated by GABAA and glycine receptors were studied in superfused cultured rat embryo spinal cord motoneurons prelabeled with [H-3]choline. AMPA elicited tritium release, possibly representing [3H]acetylcholine release in a concentration-dependent manner. The release was external Ca2+-dependent and was sensitive to Cd2+ ions, omega -conotoxin GVIA and omega -conotoxin MVIIC, but not to nifedipine, suggesting the involvement of N-, P/Q-, but not L-type Ca2+ channels. The AMPA effect was insensitive to tetrodotoxin. The glutamate receptors involved are AMPA type since the AMPA-evoked [H-3]acetylcholine release was blocked by LY303070 and was potentiated by the antidesensitizing agent cyclothiazide. Muscimol inhibited completely the AMPA effect on [H-3]acetylcholinerelease; muscimol was potentiated by diazepam and antagonized by SR95531, indicating the involvement of benzodiazepine-sensitive GABAA receptors. Glycine, acting at strychnine-sensitive receptors, also inhibited the effect of AMPA, but only in part. The inhibitory effects of muscimol and glycine are additive. We conclude that glutamate can act at AMPA receptors sited on spinal motoneurons to evoke release of acetylcholine. GABA and glycine, possibly released as cotransmitters from spinal interneurons, inhibit glutamate-evoked acetylcholine release by activating GABAA and glycine receptors on motoneurons. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 09:04:47