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Titolo:
Overactivation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate andN-methyl-D-aspartate but not kainate receptors inhibits phosphatidylcholine synthesis before excitotoxic neuronal death
Autore:
Gasull, T; DeGregorio-Rocasolano, N; Trullas, R;
Indirizzi:
CSIC, IDIBAPS, IIBB, Neurobiol Unit, Barcelona 08036, Spain CSIC Barcelona Spain 08036 IIBB, Neurobiol Unit, Barcelona 08036, Spain
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 1, volume: 77, anno: 2001,
pagine: 13 - 22
SICI:
0022-3042(200104)77:1<13:OOAA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXCITATORY AMINO-ACIDS; HIPPOCAMPAL-NEURONS; GLUTAMATE RECEPTORS; AMPA RECEPTORS; NMDA RECEPTOR; CHANNELS; RAT; CYCLOTHIAZIDE; DISORDERS; DESENSITIZATION;
Keywords:
alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate; choline; excitotoxicity; kainate; N-methyl-D-aspartate; phosphatidylcholine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Trullas, R CSIC, IDIBAPS, IIBB, Neurobiol Unit, Rossello 161, Barcelona 08036, Spain CSIC Rossello 161 Barcelona Spain 08036 Barcelona 08036, Spain
Citazione:
T. Gasull et al., "Overactivation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate andN-methyl-D-aspartate but not kainate receptors inhibits phosphatidylcholine synthesis before excitotoxic neuronal death", J NEUROCHEM, 77(1), 2001, pp. 13-22

Abstract

Glutamate receptor overactivation induces excitotoxic neuronal death, but the contribution of glutamate receptor subtypes to this excitotoxicity is unclear. We have previously shown that excitotoxicity by NMDA receptor overactivation is associated with choline release and inhibition of phosphatidylcholine synthesis. We have now investigated whether the ability of non-NMDAionotropic glutamate receptor subtypes to induce excitotoxicity is relatedto the ability to inhibit phosphatidylcholine synthesis. alpha -Amino-3-hydroxy-5-methytisoxazole-4-propionate (AMPA)-induced a concentration-dependent increase in extracellular choline and inhibited phosphatidylcholine synthesis when receptor desensitization was prevented. Kainate released cholineand inhibited phosphatidylcholine synthesis by an action at AMPA receptors, because these effects of kainate were blocked by the AMPA receptor antagonist LY300164. Selective activation of kainate receptors failed to release choline, even when kainate receptor desensitization was prevented. The inhibition of phosphatidylcholine synthesis evoked by activation of nondesensitizing AMPA receptors was followed by neuronal death. In contrast, specific kainate receptor activation, which did not inhibit phosphatidylcholine synthesis, did not produce neuronal death. Choline release and inhibition of phosphatidylcholine synthesis were induced by AMPA at non-desensitizing AMPA receptors well before excitotoxicity. Furthermore, choline release by AMPA required the entry of Ca2+ through the receptor channel. Our results show that AMPA, but not kainate, receptor overactivation induces excitotoxic celldeath, and that this effect is directly related to the ability to inhibit phosphatidylcholine synthesis. Moreover, these results indicate that inhibition of phosphatidylcholine synthesis is an early event of the excitotoxic process, downstream of glutamate receptor-mediated Ca2+ overload.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 13:05:52