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갠지하시모토,Yuko Fujita,Mao Horio,Hiroko Hagiwara,Yuko Tanibuchi,Masaomi Iyo 대한정신약물학회 2010 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.8 No.2
This study was undertaken to examine the effects of cilostazol, a selective inhibitor of type III phosphodiesterase (PDE), on hyperlocomotion and prepulse inhibition (PPI) deficits in mice after a single administration of the N-methyl-D-aspartate (NMDA)receptor antagonist dizocilpine. A single oral administration of cilostazol (0.1 and 0.3 mg/kg) significantly attenuated hyperlocomotion and PPI deficits in mice after the administration of dizocilpine (0.1 mg/kg, subcutaneously). This study suggests that cilostazol may have antipsychotic activity in animal models of schizophrenia. Therefore, cilostazol may be a potential therapeutic drug for schizophrenia, given that cilostazol has been safely used throughout the world.
Yuko Tanibuchi,Yuko Fujita,Mao Horio,Masaomi Iyo,갠지하시모토 대한정신약물학회 2010 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.8 No.3
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.
Effects of Cilostazol on Cognitive Deficits in Mice after Repeated Administration of Phencyclidine
갠지하시모토,Yuko Fujita,Tamaki Ishima,Mao Horio,Hiroko Hagiwara,Yuko Tanibuchi,Masaomi Iyo 대한정신약물학회 2010 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.8 No.1
Objective : To examine the effects of cilostazol, a selective inhibitor of type III phosphodiesterase (PDE), on cognitive deficits in mice after repeated administration of the N-methyl-D-aspartate (NMDA) receptor antagonist phencyclidine (PCP). Methods:Saline (10 ml/kg/day) or PCP (10 mg/kg/day) were administered subcutaneously to mice for 10 days (once daily on days 1−5 and 8−12). Three days (day 15) after the final administration of saline or PCP, vehicle (0.5% carboxymethylcellulose)or cilostazol (0.3, 3, 10 or 30 mg/kg/day) were administered orally for 14 consecutive days (once daily on days 15−28). The novel object recognition test (NORT) was performed 24 hours (day 29) after the final administration. Results:In the NORT, PCP -induced cognitive deficits in mice were improved significantly by subsequent sub-chronic (14 days)administration of cilostazol (3, 10 or 30 mg/kg/day), but not by the lowest dose of cilostazol (0.3 mg/kg/day). Conclusion:This study suggests that cilostazol ameliorates PCP-induced cognitive deficits in mice. Therefore, it is likely that cilostazol has therapeutic potential for cognitive deficits in schizophrenia.