Bronstein J, Farber D, Wasterlain C
Department of Neuroscience, UCLA School of Medicine 90024.
Neurochem Res. 1988 Jan;13(1):83-6. doi: 10.1007/BF00971859.
Status epilepticus was induced in paralyzed, ventilated rats using bicuculline and was maintained for 50 to 120 minutes. Cerebral cortex, hippocampus, and cerebellum were assayed for calmodulin kinase II activity in vitro using [gamma-32P]ATP and polyacrylamide gel electrophoresis. Seizures resulted in a 3.2 fold decrease in calmodulin kinase activity in crude synaptic membranes of cortex and in a 8.2 fold decrease in hippocampal membranes. Cytosolic calmodulin kinase activity was slightly increased in rats in status epilepticus but statistical significance was not reached. Status epilepticus did not affect calcium/calmodulin-dependent kinase activity in cerebellar membranes or cytosol. These data suggest that intense firing associated with continuous seizure activity decreases calmodulin kinase activity in cortical and hippocampal synaptic membranes, which may result in altered neuronal excitability.
使用荷包牡丹碱在瘫痪并通气的大鼠中诱导癫痫持续状态，并维持50至120分钟。使用[γ-32P]ATP和聚丙烯酰胺凝胶电泳在体外测定大脑皮层、海马体和小脑的钙调蛋白激酶II活性。癫痫发作导致皮层粗制突触膜中钙调蛋白激酶活性降低3.2倍，海马体膜中降低8.2倍。癫痫持续状态大鼠的胞质钙调蛋白激酶活性略有增加，但未达到统计学显著性。癫痫持续状态不影响小脑膜或胞质中的钙/钙调蛋白依赖性激酶活性。这些数据表明，与持续癫痫活动相关的强烈放电会降低皮层和海马体突触膜中的钙调蛋白激酶活性，这可能导致神经元兴奋性改变。
