The analyzes of the alteration and activity of protein kinase C in the epileptic mouse brain.

[结果] 1.戊四氮致惊厥后的变化（1）PKC活性惊厥后10 min，大脑皮质胞浆PKC活性显著高于对照组和强直惊厥组。另一方面，在皮层膜馏分惊厥后没有改变显着。戊四氮致惊厥后10 min，大鼠海马、纹状体和丘脑/下丘脑的胞浆和膜组分的PKC活性无明显变化，PKC同工酶的Western blot分析结果显示，惊厥后10 min，胞浆组分中80-KPKC β含量增加，而膜组分中80-KPKC β含量减少。在强直性惊厥期间和惊厥期后10分钟，在胞质组分中检测到50-K PkC β。PKC α和PKC β的表达相似。而惊厥后PKC γ、δ和zeta的表达无明显变化。（3）Calpain活性惊厥后皮质Calpain活性在胞浆和胞膜中无明显变化。2. EL小鼠惊厥后的变化（1）PKC同工酶表达的RT-PCR分析PKC α mRNA在惊厥间期表达较弱，惊厥后逐渐下降。PKC β在发作间期变化不大，但在发作后逐渐升高。PKC γ在发作间期表达丰富，在发作后30 min达高峰，120 min恢复到基础水平，PKC δ在发作间期表达较少，在发作后30 min达高峰。[结论]戊四氮诱导癫痫发作后，大脑皮层PKC α和PKC β由膜向胞浆转位。EL小鼠惊厥后PKC同工酶的变化与戊四氮致痫后不同。需要通过北方和蛋白质印迹分析进行进一步检查。

[RESULTS]1.The alteration after PTZ-induced convulsion(1)PKC activityThe cytosolic PKC activity in the cerebral cortex significantly increased 10 min after seizure, compared with that of the control and tonic-convulsive mouse. On the other hand, that in the cortical membrane fraction after convulsion didn't alter significantly. PTZ-induced convulsion didn't considerably change the PKC activity of the cytosolic and membrane fractions in hippocapmus, striatum and thalamus/hypothalamus.Western blot analyzes of PKC isozymesThe content of 80-K PKC beta in the cytosolic fraction increased, whereas that in the membrane fraction decreased at 10 min after convulsion. The 50-K PkC beta was detected in the cytosolic fraction during the tonic convulsion and 10 min after the convulsive phase. The expression of PKC alpha was similar to that of PKC beta. However the expressions of PKC gamma, delta, and zeta didn't alter after convulsions.(3)Calpain activityThe cortical Calpain activities in the cytosolic and membrane fraction didn't change significantly after convulsions.2.The alteration after EL mouse's seizure(1)RT-PCR analysis of PKC isozymes expressionThe mRNA expression of PKC alpha was slight at the interictal period and decreased gradually after the seizure. That of PKC beta was slight at the interictal period but increased gradually after the seizure. That of PKC gamma was abundant at the interictal period, reached a peak at 30 min after seizures and return the basal level at 120 min. That of PKC delta was little at the interictal period and peaked at 30 min after the seizure.[DISCUSSIONS]PKC alpha and beta translocated from membrane to cytosol in the cerebral cortex after PTZ-induced seizures. The alterations of PKC isozymes after seizures of EL mouse were different from those after PTZ-induced seizures. Further examinations are necessary by northern and western blot analyzes.