Dong Yu, Rosenberg Howard C
Department of Pharmacology and Therapeutics, Medical College of Ohio, 3035 Arlington Avenue, Toledo, OH 43614-5804, USA.
Neurosci Lett. 2004 Mar 4;357(2):95-8. doi: 10.1016/j.neulet.2003.11.069.
The effect of a brief pentylenetetrazol (PTZ) convulsive seizure on rat cerebral cortical Ca2+/calmodulin dependent protein kinase II (CaMKII) was investigated. By immunoblot, it was found that a single PTZ seizure, lasting less than a minute, caused translocation of CaMKII alpha-subunit (alpha-CaMKII) from the particulate to the soluble fraction for several hours, paralleled by a dramatic loss of alpha-CaMKII Thr286 phosphorylation. The reduced alpha-CaMKII Thr286 phosphorylation apparently resulted from enhanced phosphatase activity following PTZ seizure, especially in the particulate fraction. CaMKII translocation and phosphatase activation following a brief seizure episode can both contribute to long-lasting CaMKII regulation far outlasting the immediate effects of the seizure on neuronal function.
研究了短暂戊四氮（PTZ）惊厥发作对大鼠大脑皮质钙/钙调蛋白依赖性蛋白激酶II（CaMKII）的影响。通过免疫印迹发现，单次持续时间不到一分钟的PTZ惊厥发作会导致CaMKIIα亚基（α-CaMKII）在数小时内从颗粒部分转移至可溶性部分，同时α-CaMKII苏氨酸286位点的磷酸化显著减少。α-CaMKII苏氨酸286位点磷酸化减少显然是由于PTZ惊厥发作后磷酸酶活性增强所致，尤其是在颗粒部分。短暂惊厥发作后的CaMKII转移和磷酸酶激活都可能导致CaMKII的长期调节，这种调节远远超出惊厥发作对神经元功能的即时影响。
