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Titolo:
Stimulation of dopamine receptors inhibited Ca2+-calmodulin dependent protein kinase II activity in rat striatal slices
Autore:
Hou, XY; Tang, FM; Zhang, GY;
Indirizzi:
Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China Xuzhou Med Coll Xuzhou Peoples R China 221002 ou 221002, Peoples R China
Titolo Testata:
ACTA PHARMACOLOGICA SINICA
fascicolo: 11, volume: 22, anno: 2001,
pagine: 966 - 970
SICI:
0253-9756(200111)22:11<966:SODRIC>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA; PROTECTION; NEURONS; DAMAGE; DEATH; BRAIN;
Keywords:
dopamine; Ca2+-calmodulin-dependent protein kinase; anoxia; calcium; reserpine; dopamine agonists; dopamine antagonists; corpus striatum;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
14
Recensione:
Indirizzi per estratti:
Indirizzo: Zhang, GY Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China Xuzhou Med Coll Xuzhou Peoples R China 221002 Peoples R China
Citazione:
X.Y. Hou et al., "Stimulation of dopamine receptors inhibited Ca2+-calmodulin dependent protein kinase II activity in rat striatal slices", ACT PHAR SI, 22(11), 2001, pp. 966-970

Abstract

AIM: To investigate the mechanism underlying dopaminergic neurotoxicity inthe striatum during anoxia. METHODS: Using rat striatal slices as an in vitro model, the activity of Ca2+-calmodulin-dependent protein kinase II (CCDPK II) was examined by the method of substrate phosphorylation P-32-incorporation. RESULTS: Anoxia for 30 min greatly reduced CCDPK II activity by about 75 %. Reserpinization by repeated reserpine administration (1 mg (.) kg(-1) (.) d(-1) for 7 d, sc) preserved CCDPK II activity against the anoxia-induced decrease (about 40 % of control). The activity of CCDPK II was reduced significantly by exposure of rat striatal slices to micromolar concentrations of dopamine in the presence of extracellular Ca2+. Omission of Ca2+ in the incubation medium (with addition of 1 mmol/L egtazic acid) diminishedthe dopamine-induced decrease of the kinase activity. Application of apomorphine, a nonselective dopamine receptor agonist, produced a similar concentration-related decrease of CCDPK II activity. Exposure to SKF38393 (selective D-1-like receptor agonist) or quinpirole (selective D-2-like receptor agonist) also inhibited the kinase activity. The dopamine-induced decrease of CCDPK II activity was attenuated by preincubation with Sch-23390 (selective D-1-like receptor antagonist) or domperidone ( selective D-2-like receptor antagonist). CONCLUSION: Dopamine is involved in the anoxia-induced inhibition of CCDPK II activity by activation of both D-1-like and D-2-like receptors and influx of Ca2+, which may contribute to dopamine-mediated striatal neuronal damage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 23:00:32