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急性多巴胺耗竭增强体外纹状体乙酰胆碱释放中独立的刺激性和抑制性D1多巴胺受体介导的控制。

Acute dopamine depletion potentiates independent stimulatory and inhibitory D1 DA receptor-mediated control of striatal acetylcholine release in vitro.

作者信息

Login I S, Borland K, Harrison M B

机构信息

Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.

出版信息

Brain Res. 1995 May 29;681(1-2):209-12. doi: 10.1016/0006-8993(95)00295-2.

Abstract

Fractional release of [3H]ACh was evaluated under basal and evoked conditions in striatal slices from normal and acutely dopamine-depleted adult rats for the influence of D1- and D2-DA receptor agonists. The D1 ligand had no effect on normal slices but DA depletion unmasked two independent but simultaneous supersensitive responses: augmentation of K(+)-evoked and inhibition of glutamate-evoked release. The D2 ligand inhibited evoked release in normal slices and this effect was not potentiated. This is a new cholinergic model of acute D1 receptor supersensitivity.

摘要

在正常成年大鼠和急性多巴胺耗竭成年大鼠的纹状体切片中,在基础和诱发条件下评估了[3H]乙酰胆碱的分数释放,以研究D1和D2多巴胺受体激动剂的影响。D1配体对正常切片无影响,但多巴胺耗竭揭示了两个独立但同时存在的超敏反应:增强钾离子诱发的释放和抑制谷氨酸诱发的释放。D2配体抑制正常切片中的诱发释放,且这种作用未被增强。这是急性D1受体超敏反应的一种新的胆碱能模型。

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