可卡因对Fischer大鼠背纹状体ERK蛋白的诱导

Shirzad Jenab, Eugene D. Festa, Arbi Nazarian, Hui Bing K. Wu, Wei Lun Sun, Ruhal Hazim, Scott J. Russo, Vanya Quinones-Jenab
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引用次数: 57

摘要

可卡因是一种成瘾的精神兴奋剂,通过激活纹状体中多巴胺受体和多巴胺D1中的PKA通路以及谷氨酸nmda依赖机制,诱导fos和阿片基因表达。在这项研究中,我们发现单次可卡因给药可诱导Fischer大鼠尾状核/壳核中的ERK磷酸化。Phospho-ERK的增加可通过预先给药SCH23390或MK801而不是预先给药eticlopride而减少。此外,单次可卡因给药不会改变尾状核/壳核蛋白提取物中磷酸- creb蛋白或CREB-DNA结合的水平,但会增加相同提取物中磷酸- elk -1蛋白的水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cocaine induction of ERK proteins in dorsal striatum of Fischer rats

Cocaine is an addictive psychostimulant that induces fos and opioid gene expression by activating the dopamine receptors and the PKA pathways in dopamine D1 and a glutamate NMDA-dependent mechanisms in the striatum. In this study, we show that a single cocaine administration induces ERK phosphorylation in the caudate/putamen of Fischer rats. This increase in Phospho-ERK is diminished by pre-administration of SCH23390, or MK801 but not with pre-administration of eticlopride. Furthermore, this single cocaine administration does not alter the levels of phospho-CREB protein or CREB–DNA bindings in the caudate/putamen protein extracts but does increase phospho-Elk-1 protein levels in the same extracts.

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