Effects of Quetiapine on Dizocilpine-induced Prepulse Inhibition Deficits in Mice: Possible Role of the aα1 Adrenergic Receptor
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Objective: Accumulating evidence suggests that α1-adrenoceptors are involved in the mechanisms of action of some antipsychotic drugs. The purpose of this study is to examine the effects of quetiapine, an atypical antipsychotic drug with antagonist activity at α1-adrenoceptors, on prepulse inhibition (PPI) deficits in mice after a single administration of the NMDA receptor antagonist dizocilpine. Methods: Effects of quetiapine on dizocilpine-induced PPI deficits in mice were examined. Furthermore, we examined the role of α1-adrenoceptors in the mechanisms of action of quetiapine. Results: Pretreatment with quetiapine (3, 10, or 30 mg/kg, p.o.) significantly attenuated dizocilpine (0.1 mg/kg, s.c.)-induced PPI deficits in mice in a dose-dependent manner. Furthermore, dizocilpine-induced PPI deficits were also significantly ameliorated by pretreatment with the selective α1-adrenoceptor antagonist prazosin (1.0 mg/kg, p.o.). Conclusion: These findings suggest that quetiapine ameliorates dizocilpine-induced PPI deficits in mice viaα1-adrenoceptor antagonism, and hence, α1-adrenoceptor antagonism may play a prominent role in quetiapine’s psychopharmacological effects.
Abstract
Objective: Accumulating evidence suggests that α1-adrenoceptors are involved in the mechanisms of action of some antipsychotic drugs. The purpose of this study is to examine the effects of quetiapine, an atypical antipsychotic drug with antagonist activity at α1-adrenoceptors, on prepulse inhibition (PPI) deficits in mice after a single administration of the NMDA receptor antagonist dizocilpine. Methods: Effects of quetiapine on dizocilpine-induced PPI deficits in mice were examined. Furthermore, we examined the role of α1-adrenoceptors in the mechanisms of action of quetiapine. Results: Pretreatment with quetiapine (3, 10, or 30 mg/kg, p.o.) significantly attenuated dizocilpine (0.1 mg/kg, s.c.)-induced PPI deficits in mice in a dose-dependent manner. Furthermore, dizocilpine-induced PPI deficits were also significantly ameliorated by pretreatment with the selective α1-adrenoceptor antagonist prazosin (1.0 mg/kg, p.o.). Conclusion: These findings suggest that quetiapine ameliorates dizocilpine-induced PPI deficits in mice viaα1-adrenoceptor antagonism, and hence, α1-adrenoceptor antagonism may play a prominent role in quetiapine’s psychopharmacological effects.
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