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Titolo:
The activation of dopamine D4 receptors inhibits oxidative stress-induced nerve cell death
Autore:
Ishige, K; Chen, Q; Sagara, Y; Schubert, D;
Indirizzi:
Salk Inst Biol Studies, Cellular Neurobiol Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies La Jolla CA USA 92037 Lab, La Jolla, CA 92037 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 16, volume: 21, anno: 2001,
pagine: 6069 - 6076
SICI:
0270-6474(20010815)21:16<6069:TAODDR>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTATHIONE DEPLETION; GLUTAMATE TOXICITY; NEURONS; BROMOCRIPTINE; MECHANISM; CLONING; GENE;
Keywords:
HT22 cells; cell death; apomorphine; apocodeine; dopamine D4 receptors; glutamate; cGMP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Schubert, D Salk Inst Biol Studies, Cellular Neurobiol Lab, 10010 N TorreyPines Rd, La Jolla, CA 92037 USA Salk Inst Biol Studies 10010 N Torrey Pines Rd La Jolla CA USA 92037
Citazione:
K. Ishige et al., "The activation of dopamine D4 receptors inhibits oxidative stress-induced nerve cell death", J NEUROSC, 21(16), 2001, pp. 6069-6076

Abstract

Oxidative stress is thought to be the cause of nerve cell death in many CNS pathologies, including ischemia, trauma, and neurodegenerative disease. Glutamate kills nerve cells that lack ionotropic glutamate receptors via theinhibition of the cystine-glutamate antiporter x(c)(-), resulting in the inhibition of cystine uptake, the loss of glutathione, and the initiation ofan oxidative stress cell death pathway. A number of catecholamines were found to block this pathway. Specifically, dopamine and related ligands inhibit glutamate-induced cell death in both clonal nerve cell lines and rat cortical neurons. The protective effects of dopamine, apomorphine, and apocodeine, but not epinephrine and norepinephrine, are antagonized by dopamine D4antagonists. A dopamine D4 agonist also protects, and this protective effect is inhibited by U101958, a dopamine D4 antagonist. Although the protective effects of some of the catecholamines are correlated with their antioxidant activities, there is no correlation between the protective and antioxidant activities of several other ligands. Normally, glutamate causes an increase in reactive oxygen species (ROS) and intracellular Ca2+. Apomorphine partially inhibits glutamate-induced ROS production and blocks the opening of cGMP-operated Ca2+ channels that lead to Ca2+ elevation in the late part of the cell death pathway. These data suggest that the protective effects of apomorphine on oxidative stress-induced cell death are, at least in part,mediated by dopamine D4 receptors via the regulation of cGMP-operated Ca2channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 19:33:32