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为了探讨 DA耗竭对纹状体神经元缺血性损伤的保护作用是否与 Ca M K 的参与有关 ,建立了损毁大鼠黑质 +四动脉阻断前脑缺血的复合模型 ,采用同位素 3 2 P掺入法、放射自显影和 Ca M K 及磷酸化Ca M K (p- Ca M K )免疫组织化学方法 ,研究了 DA耗竭对纹状体缺血 Ca M K 活性、自身磷酸化、含量和细胞内分布的影响。发现损毁黑质、耗竭 DA可逆转由缺血引起的纹状体 Ca M K 酶活性及免疫活性下降 ,减少该酶自身磷酸化状态。这些作用可能是损毁黑质保护纹状体缺血性损伤的机制之一。
In order to investigate whether the protective effect of DA depletion on ischemic injury of striatal neurons is related to the involvement of CaMK, a composite model of forebrain ischemia in substantia nigra and four arteries was established. The model of isotonic 3 2 P Incorporation, autoradiography and CaMK and phosphorylated CaMK (p-Ca MK) immunohistochemistry were used to investigate the effect of DA depletion on striatal ischemic Ca MK activity, autophosphorylation, intracellular distribution influences. It was found that destroying the substantia nigra and depleting DA can reverse the decrease of striatal CaMK enzyme activity and immunocompetence caused by ischemia and decrease the autophosphorylation status of the enzyme. These effects may be one of the mechanisms that damage the substantia nigra to protect the ischemic injury of the striatum.