Cocaine induction of ERK proteins in dorsal striatum of Fischer rats

Molecular Brain Research Pub Date : 2005-12-14 Epub Date: 2005-11-04 DOI:10.1016/j.molbrainres.2005.08.015
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

Abstract

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.

可卡因对Fischer大鼠背纹状体ERK蛋白的诱导
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。
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