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Titolo:
Excitatory mechanisms in neuroleptic-induced vacuous chewing movements (VCMs): possible involvement of calcium and nitric oxide
Autore:
Naidu, PS; Kulkarni, SK;
Indirizzi:
Panjab Univ, Univ Inst Pharmaceut Sci, Chandigarh 160014, India Panjab Univ Chandigarh India 160014 maceut Sci, Chandigarh 160014, India
Titolo Testata:
BEHAVIOURAL PHARMACOLOGY
fascicolo: 3, volume: 12, anno: 2001,
pagine: 209 - 216
SICI:
0955-8810(200106)12:3<209:EMINVC>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR SUBUNIT EXPRESSION; CHRONIC HALOPERIDOL; TARDIVE-DYSKINESIA; DOPAMINERGIC MODULATION; EXTRACELLULAR GLUTAMATE; NEOSTRIATAL NEURONS; NMDA RECEPTOR; RATS; ASPARTATE; CLOZAPINE;
Keywords:
tardive dyskinesia; vacuous chewing movements; neuroleptics; glutamate; NMDA; calcium; nitric oxide; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Kulkarni, SK Panjab Univ, Univ Inst Pharmaceut Sci, Chandigarh 160014, India Panjab Univ Chandigarh India 160014 handigarh 160014, India
Citazione:
P.S. Naidu e S.K. Kulkarni, "Excitatory mechanisms in neuroleptic-induced vacuous chewing movements (VCMs): possible involvement of calcium and nitric oxide", BEHAV PHARM, 12(3), 2001, pp. 209-216

Abstract

Tardive dyskinesia (TD) is a serious motor side-effect of chronic neuroleptic therapy. Chronic treatment with neuroleptics leads to the development of oral abnormal movements in rats known as vacuous chewing movements (VCMs), Vacuous chewing movements in rats have been widely accepted as an animal model of tardive dyskinesia, Chronic blockade of D-2 inhibitory dopamine (DA) receptors localized on glutamatergic terminals in the striatum leads to the persistent enhanced release of glutamate that kills the striatal outputneurons. The object of the present study was to explore the role of glutamatergic modulation on the neuroleptic-induced VCMs, Rats were chronically (for 21 days) treated with haloperidol (1.5 mg/ kg, i,p,) to produce VCMs. The neuroleptic-induced VCMs viz,, vertical jaw movements, tongue protrusions and bursts of jaw tremors, were counted during a 5 min observation period. Dizocilpine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, dose dependently (0.02 and 0.05 mg/kg) reduced haloperidol-induced VCMs. Felodipine (5 and 10 mg/kg), an L-type calcium-channel blocker, also significantly reduced the VCM count. N-omega-nitro-L-arginine methyl ester (L-NAME) (25 and 50 mg/ kg), a nitric oxide synthase inhibitor, also reducedthe VCM count in an L-arginine-sensitive manner. In conclusion, the findings of the present study indicated NMDA receptor involvement in haloperidol-induced VCMs, and also suggested the possible involvement of calcium and nitric oxide in haloperidol-induced VCMs, (C) 2001 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 08:01:17