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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Enhancement of dopamine-induced signaling responses in the forebrain of mice lacking dopamine D3 receptor.
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Enhancement of dopamine-induced signaling responses in the forebrain of mice lacking dopamine D3 receptor.

机译:缺乏多巴胺D3受体的小鼠的前脑中多巴胺诱导的信号反应的增强。

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摘要

It is well known that the dopamine D(3) receptor plays a critical role in several psychological disorders, such as drug dependence. The present study was designed to investigate the influence of lacking dopamine D(3) receptors in dopamine-induced G-protein activation and Ca(2+) influx in the mouse forebrain. The deletion of dopamine D(3) receptor gene caused the enhancement of dopamine-induced G-protein activation in the limbic forebrain of dopamine D(3) receptor knockout (D(3)KO) mice. Furthermore, the dopamine-induced Ca(2+) influx was enhanced in the coculture of neuron/glia cells obtained from the forebrain of D(3)KO mice. The present data provide direct evidence that a deletion of central dopamine D(3) receptor enhances the dopamine D(1)/D(2) receptor-mediated intracellular signaling.
机译:众所周知,多巴胺D(3)受体在几种心理疾病(例如药物依赖性)中起着至关重要的作用。本研究旨在调查缺乏多巴胺D(3)受体在小鼠前脑多巴胺诱导的G蛋白活化和Ca(2+)流入的影响。多巴胺D(3)受体基因的缺失导致多巴胺D(3)受体基因敲除(D(3)KO)小鼠的边缘前脑中多巴胺诱导的G蛋白活化增强。此外,在从D(3)KO小鼠的前脑获得的神经元/神经胶质细胞的共培养中,多巴胺诱导的Ca(2+)流入量增加。本数据提供直接证据表明,中央多巴胺D(3)受体的缺失增强了多巴胺D(1)/ D(2)受体介导的细胞内信号传导。

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