大鼠纹状体喹啉酸损伤可消除D1和D2多巴胺受体介导的僵住症。
Quinolinic acid lesions of rat striatum abolish D1- and D2-dopamine receptor-mediated catalepsy.
作者信息
Calderon S F, Sanberg P R, Norman A B
机构信息
Department of Psychiatry, University of Cincinnati College of Medicine, OH 45267.
出版信息
Brain Res. 1988 May 31;450(1-2):403-7. doi: 10.1016/0006-8993(88)91584-3.
The selective D1-dopamine receptor antagonist SCH23390 and the more D2-selective antagonist haloperidol produced marked catalepsy in rats. The novel excitotoxin quinolinic acid (QA) selectively destroys striatal neurons when injected directly into the striatum. Bilateral QA lesions of the rat striatum (150 nmol and 225 nmol per side) abolished the cataleptic response to both SCH23390 and haloperidol. These data indicate that the D1- and/or D2-dopamine receptors which mediate the cataleptic response are restricted to QA-sensitive neurons in the rat striatum.
选择性D1-多巴胺受体拮抗剂SCH23390和更具D2选择性的拮抗剂氟哌啶醇在大鼠中产生明显的僵住症。新型兴奋性毒素喹啉酸（QA）直接注射到纹状体时可选择性地破坏纹状体神经元。大鼠纹状体的双侧QA损伤（每侧150 nmol和225 nmol）消除了对SCH23390和氟哌啶醇的僵住症反应。这些数据表明，介导僵住症反应的D1和/或D2多巴胺受体仅限于大鼠纹状体中对QA敏感的神经元。
Zotero 插件