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抗精神病药物所致僵住症作为帕金森病的一种模型。I. 多巴胺能药物的作用

Neuroleptic-induced catalepsy as a model of Parkinson's disease. I. Effect of dopaminergic agents.

作者信息

Elliott P J, Close S P, Walsh D M, Hayes A G, Marriott A S

机构信息

Glaxo Group Research Ltd., Neuropharmacology Department, Ware, Hertfordshire, United Kingdom.

出版信息

J Neural Transm Park Dis Dement Sect. 1990;2(2):79-89. doi: 10.1007/BF02260896.

Abstract

Catalepsy was observed in the rat following intrastriatal injections of the dopamine antagonists sulpiride or fluphenazine and after subcutaneous administration of fluphenazine. The neuroleptic-induced catalepsy was reversed by the classical anti-parkinsonian agent L-DOPA and by agents that function through dopamine systems such as d- and methamphetamine and the direct D2 receptor agonist quinpirole. The D1 agonist SKF 38393, and the D1/D2 agonist apomorphine, were ineffective in this model. These results support limited use of the rat catalepsy model for the screening of potential anti-parkinsonian compounds and indicate that this procedure can provide valuable information concerning striatal dopamine function.

摘要

在大鼠纹状体内注射多巴胺拮抗剂舒必利或氟奋乃静以及皮下注射氟奋乃静后,观察到了僵住症。经典的抗帕金森病药物左旋多巴以及通过多巴胺系统起作用的药物(如右旋苯丙胺和甲基苯丙胺)和直接的D2受体激动剂喹吡罗可逆转抗精神病药物诱发的僵住症。D1激动剂SKF 38393和D1/D2激动剂阿扑吗啡在该模型中无效。这些结果支持有限度地使用大鼠僵住症模型来筛选潜在的抗帕金森病化合物,并表明该程序可以提供有关纹状体多巴胺功能的有价值信息。

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