Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Regulation of NMDA-stimulated [C-14]GABA and [H-3]acetylcholine release bystriatal glutamate and dopamine receptors
Autore:
Hanania, T; Johnson, KM;
Indirizzi:
Univ Texas, Med Branch, Dept Pharmacol & Toxicol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 acol & Toxicol, Galveston, TX 77555 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 844, anno: 1999,
pagine: 106 - 117
SICI:
0006-8993(19991009)844:1-2<106:RON[A[>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXCITATORY AMINO-ACID; PROTEIN-KINASE-C; D-ASPARTATE RECEPTORS; PHENCYCLIDINE-LIKE DRUGS; RAT STRIATUM; NEUROTRANSMITTER RELEASE; PHENYLGLYCINE DERIVATIVES; TURNING BEHAVIOR; XENOPUS OOCYTES; NERVE-TERMINALS;
Keywords:
ACh release; dopamine; GABA release; glutamate; NMDA; striatum; Parkinson's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Johnson, KM Univ Texas, Med Branch, Dept Pharmacol & Toxicol, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 ol, Galveston, TX 77555 USA
Citazione:
T. Hanania e K.M. Johnson, "Regulation of NMDA-stimulated [C-14]GABA and [H-3]acetylcholine release bystriatal glutamate and dopamine receptors", BRAIN RES, 844(1-2), 1999, pp. 106-117

Abstract

Striatal function is heavily influenced by glutamatergic and dopaminergic afferent input. To ultimately better understand how the N-methyl-D-aspartate (NMDA) antagonist, phencyclidine (PCP), alters striatal function, we sought to determine how NMDA receptor function is influenced by activation of other glutamatergic receptors and by dopaminergic receptors. To this end, weused NMDA-stimulated efflux of [C-14]GABA and [H-3]acetylcholine (ACh) from striatal slices to assess the influence of these receptors on NMDA function. NMDA-stimulated [C-14]GABA release was more sensitive to NMDA and glycine antagonists than was [H-3]ACh release, suggesting that different NMDA receptors regulate the release of these neurotransmitters. Furthermore, NMDA-stimulated [H-3]ACh release was inhibited by a D-2 receptor mechanism whereas NMDA-stimulated [C-14]GABA release was enhanced by D-1 receptor activation. NMDA and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acidhydrobromide (AMPA) interact additively to evoke [H-3]ACh release, and synergistically to evoke [C-14]GABA release. An additive effect of NMDA and kainate (KA) was found on [C-14]GABA release, but NMDA and KA. acted in a less than additive manner in evoking [H-3]ACh release. KA-stimulated [H-3]ACh release was largely blocked by NMDA antagonists, suggesting mediation through activation of NMDA receptors, probably secondary to KA-induced glutamaterelease. A selective group II metabotropic receptor agonist inhibited NMDA-stimulated [C-14]GABA and [H-3]ACh release. On the other hand, NMDA-stimulated [C-14]GABA release was potentiated by activation of group I metabotropic receptors. Thus, in addition to the differential modulation by D-1- and D-2-like receptors, the release of striatal neurotransmitters by NMDA receptor activation depends on the extent to which the other glutamate receptors, both ionotropic and metabotropic, are activated. (C) 1999 Published by Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 03:28:49