Efeito da anandamida nos movimentos de mascar no vazio induzidos por haloperidol em ratos: participação do receptor CB1
Treatment with antipsychotic drugs may cause tardive dyskinesia in humans and orofacial dyskinesia in rodents. Although the dopaminergic system in basal ganglia has been implicated in these movement disorders, their underlying mechanisms remain unclear. In recent years, the identification of high de...
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| Tipo de recurso: | tesis de maestría |
| Estado: | Versión publicada |
| Fecha de publicación: | 2012 |
| País: | Brasil |
| Institución: | Universidade Federal de Santa Maria (UFSM) |
| Repositorio: | Manancial - Repositório Digital da UFSM |
| Idioma: | portugués |
| OAI Identifier: | oai:repositorio.ufsm.br:1/9005 |
| Acceso en línea: | http://repositorio.ufsm.br/handle/1/9005 |
| Access Level: | acceso abierto |
| Palabra clave: | Endocanabinóides Anandamida Sistema dopaminérgico Discinesia tardia Endocannabinoids Anandamide Dopaminergic system Tardive dyskinesia CNPQ::CIENCIAS BIOLOGICAS::FARMACOLOGIA |
| Sumario: | Treatment with antipsychotic drugs may cause tardive dyskinesia in humans and orofacial dyskinesia in rodents. Although the dopaminergic system in basal ganglia has been implicated in these movement disorders, their underlying mechanisms remain unclear. In recent years, the identification of high density of CB1 cannabinoid receptors within the basal ganglia has suggested a potential role for endocannabinoids in the control of basal ganglia-related movement disorders. Thus, the present study aimed to investigate whether CB1 receptors are involved in haloperidol-induced orofacial dyskinesia in rats. Adult male rats were treated with haloperidol decanoate (38 mg/kg, i.m., single administration). After 24 days, the animals were submitted to stereotaxic surgery for insertion of cannulas on right ventricle. After recovery, the effect of anandamide (6 nmol, i.c.v.) and/or the CB1 receptor antagonist SR141716A (30 μg, i.c.v.) on haloperidol-induced VCMs was assessed. Anandamide reversed haloperidol-induced VCMs. SR141716A (30 μg, i.c.v.) did not alter haloperidol-induced VCM per se, but prevented the effect of anandamide on VCM in rats. In conclusion, our results show that activation of CB1 receptor may prevent haloperidol-induced VCMs in rats, implicating cannabinoid signaling via CB1 receptor in orofacial dyskinesia. |
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