杏仁核点燃引发百日咳毒素催化的ADP-核糖基化的持续变化。

Amygdaloid kindling elicits persistent changes in pertussis toxin-catalyzed ADP-ribosylation.

作者信息

Iwasa H, Hasegawa S, Kikuchi S, Watanabe K, Sato T

机构信息

Department of Neuropsychiatry, Faculty of Medicine, Chiba University, Japan.

出版信息

Epilepsia. 1994 Jul-Aug;35(4):855-60. doi: 10.1111/j.1528-1157.1994.tb02523.x.

DOI:10.1111/j.1528-1157.1994.tb02523.x

PMID:8082634

Abstract

We examined the changes in pertussis toxin (PTX)-catalyzed ADP-ribosylation in amygdaloid-kindled rats to clarify the role of G proteins in the basic mechanisms of epilepsies. Autoradiographic analysis showed a remarkable increase in PTX-catalyzed ADP-ribosylation in 39-41-kDa proteins in hippocampus and cerebral cortex of kindled animals. The 39- to 41-kDa proteins were shown to be alpha-subunits of Gi and Go by immunoblotting with specific anti-Gi alpha and anti-Go alpha. The increase in ADP-ribosylation of these proteins was observed on stimulated and unstimulated sides of brains 24 h after the last generalized seizure and persisted for at least 3-4 weeks. These results suggest that persistent alterations in signal transduction through Gi and Go might be related to acquisition of long-lasting epileptogenesis.

摘要

我们检测了杏仁核点燃大鼠中百日咳毒素（PTX）催化的ADP核糖基化变化，以阐明G蛋白在癫痫基本机制中的作用。放射自显影分析显示，点燃动物海马和大脑皮层中39 - 41 kDa蛋白的PTX催化的ADP核糖基化显著增加。通过用特异性抗Giα和抗Goα进行免疫印迹，证实39至41 kDa蛋白为Gi和Go的α亚基。在最后一次全身性癫痫发作后24小时，在大脑的刺激侧和未刺激侧均观察到这些蛋白的ADP核糖基化增加，并持续至少3 - 4周。这些结果表明，通过Gi和Go的信号转导的持续改变可能与持久癫痫发生的获得有关。