Imai S, Onozuka M
Department of Anatomy, Gifu University School of Medicine, Japan.
Epilepsy Res. 1991 Mar;8(2):95-101. doi: 10.1016/0920-1211(91)90076-r.
In cobalt-induced epileptogenic cortex in rats, a marked increase in two proteins of about 84 kDa and 70 kDa, a slight increase in 12-kDa and 10-kDa proteins and a decrease in a protein of about 57 kDa were noted, as determined by SDS-polyacrylamide gel electrophoresis. The initiation of these protein changes was ahead of the generation of epileptogenic activities. The anticonvulsant drugs phenytoin (PHT) and phenobarbital (PB) attenuated the cobalt-induced epileptogenic activities, but failed to suppress the protein changes. Among these proteins, a 70-kDa protein, when injected intracortically into the motor region of the normal rat cerebrum, evoked epileptic discharges on the electrocorticograph and behavioral seizure, which were abolished by prior treatment with PHT or PB. These findings suggest that the above protein changes are not an indirect offshoot of secondary stimulation of neurons by neurotransmitters or neuromodulators, and that P70 may contribute to the generation of epileptic seizure activities.
通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳测定发现，在钴诱导的大鼠致痫皮层中，约84 kDa和70 kDa的两种蛋白质显著增加，12 kDa和10 kDa的蛋白质略有增加，约57 kDa的一种蛋白质减少。这些蛋白质变化的起始早于致痫活动的产生。抗惊厥药物苯妥英（PHT）和苯巴比妥（PB）可减弱钴诱导的致痫活动，但未能抑制蛋白质变化。在这些蛋白质中，一种70 kDa的蛋白质，当皮层内注射到正常大鼠大脑的运动区域时，会在脑电图上诱发癫痫放电和行为性癫痫发作，而预先用PHT或PB治疗可消除这些症状。这些发现表明，上述蛋白质变化并非神经递质或神经调质对神经元二次刺激的间接结果，并且P70可能有助于癫痫发作活动的产生。
