Effects of haloperidol and GM 1 ganglioside treatment on striatal D 2 receptor binding and dopamine turnover

Abstract

Previous studies have shown that whereas exogenous GM 1 ganglioside co-administration leads to an increase of haloperidol-induced behavioral supersensitivity, GM 1 significantly attenuates the behavioral parameters of dopaminergic supersensitivity when administered after abrupt haloperidol withdrawal. In the present study, the effects of GM 1 and haloperidol co-administration (5 mg/kg GM 1 i.p. and 1 mg/kg haloperidol i.p., twice daily, for 30 days) as well as the effects of a 3 day treatment with GM 1 were investigated in rats withdrawn from haloperidol administration by measuring striatal D 2 dopamine receptor binding and dopamine turnover. The results showed that under these two experimental conditions GM 1 modified neither the haloperidol-induced striatal D 2 dopamine receptor up regulation nor the decrease in dopamine turnover produced by haloperidol withdrawal. These results suggest that the effects of GM 1 on behavioral supersensitivity are not related to modifications in dopamine receptor number or affinity and in the synaptic availability of this catecholamine.