• Jivago Röpke, Alcindo Busanello, Caroline Queiroz Leal, Elizete de Moraes Reis, Catiuscia Molz de Freitas, Jardel Gomes Villarinho, Fernanda Hernandes Figueira, Carlos Fernando Mello, Juliano Ferreira, and Roselei Fachinetto.
• Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, RS, Brazil.
• Prog. Neuropsychopharmacol. Biol. Psychiatry. 2014 Oct 3; 54: 195-9.

AbstractAntipsychotics may cause tardive dyskinesia in humans and orofacial dyskinesia in rodents. Although the dopaminergic system has been implicated in these movement disorders, which involve the basal ganglia, their underlying pathomechanisms remain unclear. CB1 cannabinoid receptors are highly expressed in the basal ganglia, and a potential role for endocannabinoids in the control of basal ganglia-related movement disorders has been proposed. Therefore, this study investigated whether CB1 receptors are involved in haloperidol-induced orofacial dyskinesia in rats. Adult male rats were treated for four weeks with haloperidol decanoate (38mg/kg, intramuscularly - i.m.). The effect of anandamide (6nmol, intracerebroventricularly - i.c.v.) and/or the CB1 receptor antagonist SR141716A (30μg, i.c.v.) on haloperidol-induced vacuous chewing movements (VCMs) was assessed 28days after the start of the haloperidol treatment. Anandamide reversed haloperidol-induced VCMs; SR141716A (30μg, i.c.v.) did not alter haloperidol-induced VCM per se but prevented the effect of anandamide on VCM in rats. These results suggest that CB1 receptors may prevent haloperidol-induced VCMs in rats, implicating CB1 receptor-mediated cannabinoid signaling in orofacial dyskinesia.Copyright © 2014. Published by Elsevier Inc.

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