Chronic, systemic treatment with a metabotropic @entity2227 receptor 5 antagonist produces anxiolytic-like effects and reverses abnormal firing activity of projection neurons in the basolateral nucleus of the amygdala in XXXX with bilateral @entity2955 lesions.

@entity2227 @entity146 @entity12369 @entity12370 @entity191 @entity3826 @entity148 @entity35 @entity669 @entity2955
Although @entity12369 ( @entity12370 ), a selective metabotropic @entity2227 receptor 5 antagonist, improves the motor symptoms of @entity191 ( @entity191 ), the effects of @entity12370 on the psychiatric symptom of @entity191 and the mechanism involved are still unclear. In the present study, we examined the effects of @entity12370 in anxiolytic-like behavior and firing activity of projection neurons in the basolateral nucleus of the amygdala (BLA) in @entity35 with @entity2955 ( @entity2955 ) injected bilaterally into dorsal striatum. @entity35 were divided into three groups, sham-operated group, @entity2955 lesion with vehicle treatment group and @entity2955 lesion with @entity12370 treatment group. Injection of @entity2955 (10.5  g) into the dorsal striatum produced 31.5% loss of @entity669 hydroxylase immunoreactive (TH-ir) neurons in the SNpc. The @entity2955 -lesioned @entity35 showed @entity146 and the firing rate of BLA projection neurons decreased significantly compared with sham-operated @entity35 , and no difference was found in the firing pattern of these neurons. Whereas chronic, systemic treatment of @entity12370 (3 mg/kg/day, i.p.; 14 days) attenuated loss of TH-ir neurons, produced anxiolytic-like effect and normalized the abnormal firing rate of projection neurons of the BLA in @entity35 with the bilateral lesions. Systemic administration of cumulative @entity3826 (10-160  g/kg, i.v.) inhibited the firing rate of BLA projection neurons in sham-operated, @entity2955 lesion with vehicle-treated and @entity12370 -treated @entity35 , but the @entity2955 lesion decreased the response of BLA projection neurons to @entity3826 stimulation, while @entity12370 reversed the reactivity of these neurons. These data demonstrate that the partial lesion of the nigrostriatal pathway causes @entity148 symptom and decreases firing rate of BLA projection neurons in the @entity35 . Furthermore, chronic, systemic @entity12370 treatment has the neuroprotective and anxiolytic-like effects, and reverses the abnormal firing rate of BLA projection neurons, suggesting that @entity12370 has important implication for the treatment of @entity191 .
