RESUMO
Using vacuous chewing movement(VCM) of rats as a possible animal model for tardive dyskinesia(TD), we tried to investigate the effects of haloperidol decanoate treatment on the rat brain: VCM(+) incidence, and morphological and neurochemical effect in the VCM(+) group. In our study, there were three treatment schedules of vehicle or haloperidol decanoate: 4, 7 or 9 total number of injections of vehicle or haloperidol decanoate were administered over 9, 18 or 24 weeks, respectively, with an injection given every 3 weeks. We rated VCM scores of rats at each injection time. Haloperidol groups were then further divided into VCM(-) rats and VCM(+) rats according to their VCM scores. Afterward, VCM(+) incidence was obtained in each haloperidol group. As time of neuroleptic treatment increased, the VCM scores and incidence of VCM(+) were found to be increased. All of the control, VCM(+) and VCM(-) rats were sacrificed to determine if treatments had morphological and neurochemical effects in the brain. Density of medium-sized neurons and levels of GABA in the striatum were reduced in the VCM(+) group 3 with total 9 injections given, compared to either VCM(-) group 3 or control group 3. These results suggest that hypofunction of GABAnergic neurons is associated with the development of VCM and possibly, TD.
Assuntos
Animais , Ratos , Agendamento de Consultas , Encéfalo , Ácido gama-Aminobutírico , Ácido Glutâmico , Haloperidol , Incidência , Mastigação , Modelos Animais , NeurôniosRESUMO
Using vacuous chewing movement(VCM) of rats as a possible animal model for tardive dyskinesia(TD), we tried to investigate the effects of haloperidol decanoate treatment on the rat brain: VCM(+) incidence, and morphological and neurochemical effect in the VCM(+) group. In our study, there were three treatment schedules of vehicle or haloperidol decanoate: 4, 7 or 9 total number of injections of vehicle or haloperidol decanoate were administered over 9, 18 or 24 weeks, respectively, with an injection given every 3 weeks. We rated VCM scores of rats at each injection time. Haloperidol groups were then further divided into VCM(-) rats and VCM(+) rats according to their VCM scores. Afterward, VCM(+) incidence was obtained in each haloperidol group. As time of neuroleptic treatment increased, the VCM scores and incidence of VCM(+) were found to be increased. All of the control, VCM(+) and VCM(-) rats were sacrificed to determine if treatments had morphological and neurochemical effects in the brain. Density of medium-sized neurons and levels of GABA in the striatum were reduced in the VCM(+) group 3 with total 9 injections given, compared to either VCM(-) group 3 or control group 3. These results suggest that hypofunction of GABAnergic neurons is associated with the development of VCM and possibly, TD.