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电惊厥休克导致肌酸激酶活性降低。

Decreased creatine kinase activity caused by electroconvulsive shock.

作者信息

Búrigo Márcio, Roza Clarissa A, Bassani Cintia, Feier Gustavo, Dal-Pizzol Felipe, Quevedo João, Streck Emilio L

机构信息

Laboratório de Bioquímica Experimental, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil.

出版信息

Neurochem Res. 2006 Jul;31(7):877-81. doi: 10.1007/s11064-006-9091-1. Epub 2006 Jun 21.

Abstract

Although several advances have occurred over the past 20 years concerning the use and administration of electroconvulsive therapy to minimize side effects of this treatment, little progress has been made in understanding its mechanism of action. Creatine kinase is a crucial enzyme for brain energy homeostasis, and a decrease of its activity has been associated with neuronal death. This work was performed in order to evaluate creatine kinase activity from rat brain after acute and chronic electroconvulsive shock. Results showed an inhibition of creatine kinase activity in hippocampus, striatum and cortex, after acute and chronic electroconvulsive shock. Our findings demonstrated that creatine kinase activity is altered by electroconvulsive shock.

摘要

尽管在过去20年里,在电休克治疗的使用和管理方面取得了一些进展,以尽量减少这种治疗的副作用,但在了解其作用机制方面进展甚微。肌酸激酶是维持脑能量稳态的关键酶,其活性降低与神经元死亡有关。进行这项研究是为了评估急性和慢性电休克后大鼠脑内肌酸激酶的活性。结果显示,急性和慢性电休克后,海马体、纹状体和皮质中的肌酸激酶活性受到抑制。我们的研究结果表明,电休克会改变肌酸激酶的活性。

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