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Titolo:
Nitric oxide synthase inhibitors cause motor deficits in mice
Autore:
Araki, T; Mizutani, H; Matsubara, M; Imai, Y; Mizugaki, M; Itoyama, Y;
Indirizzi:
Tohoku Univ, Grad Sch Sci & Med, Dept Clin Pharmacol & Therapeut, Aoba Ku,Sendai, Miyagi 9808578, Japan Tohoku Univ Sendai Miyagi Japan 9808578 Ku,Sendai, Miyagi 9808578, Japan Tohoku Univ Hosp, Dept Pharmaceut Sci, Sendai, Miyagi, Japan Tohoku Univ Hosp Sendai Miyagi Japan armaceut Sci, Sendai, Miyagi, Japan Tohoku Univ, Sch Med, Dept Internal Med 2, Sendai, Miyagi 980, Japan Tohoku Univ Sendai Miyagi Japan 980 rnal Med 2, Sendai, Miyagi 980, Japan Tohoku Univ, Sch Med, Dept Neurol, Sendai, Miyagi 980, Japan Tohoku Univ Sendai Miyagi Japan 980 ept Neurol, Sendai, Miyagi 980, Japan
Titolo Testata:
EUROPEAN NEUROPSYCHOPHARMACOLOGY
fascicolo: 2, volume: 11, anno: 2001,
pagine: 125 - 133
SICI:
0924-977X(200104)11:2<125:NOSICM>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL CEREBRAL-ISCHEMIA; MPTP NEUROTOXICITY; MONOAMINE-OXIDASE; 7-NITRO INDAZOLE; DOPAMINE RELEASE; RAT-BRAIN; CATALEPSY; PARKINSONISM; INCREASES; BEHAVIOR;
Keywords:
7-nitroindazole; L-NAME; haloperidol; motor behaviour; nitric oxide synthase inhibitor; dopamine content; mice;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Araki, T Tohoku Univ, Grad Sch Sci & Med, Dept Clin Pharmacol & Therapeut,Aoba Ku,Sendai, Miyagi 9808578, Japan Tohoku Univ Sendai Miyagi Japan 9808578 i, Miyagi 9808578, Japan
Citazione:
T. Araki et al., "Nitric oxide synthase inhibitors cause motor deficits in mice", EUR NEUROPS, 11(2), 2001, pp. 125-133

Abstract

We investigated possible motor effects of 7-nitroindazole (7-NI), an neuronal nitric oxide synthase (nNOS) inhibitor, and N-G-nitro-L-arginine methylester (L-NAME), an non-selective NOS inhibitor in mice using catalepsy andpole tests in comparison with dopamine D-2 receptor antagonist, haloperidol. We also studied the change in dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (I-IVA) contents: of these compounds. The administration of 7-NI and L-NAME (40-160 mg/kg, s.c.) dose-dependently inducedmotor deficit in both catalepsy anti pole tests. The motor deficit inducedby 7-NI was more pronounced than the one produced by L-NAME. In contrast, haloperidol showed a marked motor deficit in mice. Haloperidol showed a marked motor deficit as compared with 7-NI and I.-NAME. For dopamine, DOPAC and HVA contents, haloperidol exhibited a significant decrease in dopamine content and a significant increase in DOPAC and HVA content in the striatum. In contrast, 7-NI showed a significant increase in the striatal dopamine content. However, 7-N1 had no significant change in the striatal DOPAC and HVA contents. On the other hand, no significant change in the striatal dopamine, DOPAC and HVA contents was observed in L-NAME-treated mice. The presentstudy also showed that the motor deficit induced by 7-NI or L-NAME was significantly attenuated by the treatment with L-arginine. These results demonstrate that NOS inhibitors as well as dopamine D-2 receptor antagonist haloperidol can induce motor deficit in mice. The present study also suggests that the mechanism in the motor deficit caused by NOS inhibitors may be different from that in the motor deficit induced by haloperidol. Furthermore, our findings suggest that nNOS may play some role in control of motor behavior. (C) 2001 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 20/06/19 alle ore 17:00:19