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目的:研究多巴胺(DA)耗竭对纹状体缺血后DARPP-32蛋白磷酸化水平、细胞内分布和mRNA表达的影响,探讨DA在缺血性纹状体损伤中的作用机制。方法:采用6-羟基多巴胺损毁大鼠黑质和四血管阻断全脑缺血模型,用放射自显影、免疫组化和原位杂交的方法观察DARPP-32的含量、磷酸化水平及mRNA表达情况的变化。结果:缺血后体外测定DARPP-32[~(32)P]的掺入量降低。黑质损毁后再缺血,损毁侧纹状体DARPP-32[λ-~(32)P]掺入量有明显升高,且DARPP-32免疫反应阳性神经元及mRNA表达均明显强于对照侧。结论:纹状体缺血时DARPP-32体内磷酸化增加,而耗竭DA可抑制这种作用。黑质损毁可升高纹状体缺血时DARPP-32免疫反应性及DARPP-32mRNA的表达水平。
Objective: To investigate the effect of dopamine (DA) depletion on the phosphorylation of DARPP-32 protein, intracellular distribution and mRNA expression after striatal ischemia, and to explore the mechanism of DA in ischemic striatum. Methods: The model of global cerebral ischemia was induced by 6-hydroxydopamine-lesioned substantia nigra and four-vessel occlusion in rats. The contents of DARPP-32, phosphorylation and mRNA expression were observed by autoradiography, immunohistochemistry and in situ hybridization Changes in the situation. Results: The amount of DARPP-32 [~ (32) P] was decreased in vitro after ischemia. DALPP-32 [λ- ~ (32) P] incorporation was significantly increased after ischemic necrosis of substantia nigra, and the expression of DARPP-32 immunoreactive neurons and mRNA were significantly higher than that of the control side. CONCLUSIONS: DARPP-32 phosphorylation is increased in striatum during ischemia, whereas depletion of DA inhibits this effect. Nigral damage can increase the striatal ischemia DARPP-32 immunoreactivity and DARPP-32 mRNA expression levels.