Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Effects of glutathione depletion by 2-cyclohexen-1-one on excitatory aminoacids-induced enhancement of activator protein-1 DNA binding in murine hippocampus
Autore:
Ogita, K; Kitayama, T; Okuda, H; Yoneda, Y;
Indirizzi:
Setsunan Univ, Fac Pharmaceut Sci, Dept Pharmacol, Osaka 5730101, Japan Setsunan Univ Osaka Japan 5730101 , Dept Pharmacol, Osaka 5730101, Japan Kanazawa Univ, Fac Pharmaceut Sci, Dept Mol Pharmacol, Kanazawa, Ishikawa,Japan Kanazawa Univ Kanazawa Ishikawa Japan harmacol, Kanazawa, Ishikawa,Japan
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 6, volume: 76, anno: 2001,
pagine: 1905 - 1915
SICI:
0022-3042(200103)76:6<1905:EOGDB2>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYL-D-ASPARTATE; NMDA RECEPTOR ACTIVATION; CEREBELLAR GRANULE CELLS; KAINIC ACID; RAT-BRAIN; NITRIC-OXIDE; TRANSCRIPTION FACTORS; OXIDIZED GLUTATHIONE; CEREBRAL GLUTATHIONE; INTRACELLULAR CA2+;
Keywords:
activator protein-1; 2-cyclohexen-1-one; DNA binding; glutathione; kainic acid; N-methyl-D-aspartic acid;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Ogita, K Setsunan Univ, Fac Pharmaceut Sci, Dept Pharmacol, 45-1 NagaotogeCho, Osaka 5730101, Japan Setsunan Univ 45-1 Nagaotoge Cho Osaka Japan 5730101 0101, Japan
Citazione:
K. Ogita et al., "Effects of glutathione depletion by 2-cyclohexen-1-one on excitatory aminoacids-induced enhancement of activator protein-1 DNA binding in murine hippocampus", J NEUROCHEM, 76(6), 2001, pp. 1905-1915

Abstract

We have investigated the role of glutathione in mechanisms associated withexcitatory amino acid signaling to the nuclear transcription factor activator protein-1 (AP1) in the brain using mice depleted of endogenous glutathione by prior treatment with 2-cyclohexen-1-one (CHX). In the hippocampus ofanimals treated with CHX 2 h before, a significant increase was seen in enhancement of AP1 DNA binding When determined 2 h after the injection of kainic acid (KA) at low doses. The sensitization to KA was not seen in animalsinjected with CHX 24 h before, in coincidence with the recovery of glutathione contents to the normal revels. By contrast, CHX did not significantly affect the potentiation by NMDA of API binding under-any experimental conditions. Prior treatment with CHX resulted in facilitation of behavioral changes induced by KA without affecting those induced by NMDA. These results suggest that endogenous glutathione may be at least in part involved in molecular mechanisms underlying transcriptional control by KA, but not by NMDA, signals of cellular functions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 04:28:47