Alterations of protein kinase C in rat hippocampus following traumatic brain injury.
Alterations of protein kinase C in rat hippocampus following traumatic brain injury.
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DOI：
10.1089/neu.1993.10.287
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发表时间：
1993
影响因子：
4.2
通讯作者：
Keyi Yang;WILLIAM C. Taft;C. Dixon;CARLO A. Todaro;ROBERT K. Yu;Ronald L. Hayes
中科院分区：
文献类型：
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作者：
Keyi Yang;WILLIAM C. Taft;C. Dixon;CARLO A. Todaro;ROBERT K. Yu;Ronald L. Hayes
钙依赖性兴奋性毒性过程在创伤性脑损伤（TBI）的病理反应中起重要作用。TBI引起神经元去极化和过度兴奋性神经递质释放，这可能导致细胞内钙水平增加。然而，TBI后钙依赖性酶如蛋白激酶C（PKC）的反应知之甚少。由于PKC在信号转导和维持正常神经功能中起着重要作用，我们研究了大鼠液压脑损伤后PKC活性和蛋白水平的变化。伤后1小时PKC活性增加23.1%，伤后3小时增加80.7%。伤后5min和24h PKC活性无明显变化。PKC免疫标记的研究发现，PKC水平的膜组分3小时，但不是1小时后损伤显着增加。因此，PKC激活短暂增加TBI后，可能发挥重要作用的病理生理反应TBI。
Calcium-dependent excitotoxic processes contribute significantly to pathologic responses to traumatic brain injury (TBI). TBI causes neuronal depolarization and excessive excitatory neurotransmitter release, which may lead to increases in intracellular calcium levels. However, responses of calcium-dependent enzymes such as protein kinase C (PKC) following TBI are poorly understood. Since PKC plays an important role in signal transduction and maintenance of normal neuronal function, we investigated changes in PKC activity and protein levels following fluid percussion brain injury in rats. We observed a 23.1% increase in PKC activity 1 h postinjury and 80.7% increase in PKC activity 3 h postinjury. There was no statistically significant change in PKC activity 5 min and 24 h after injury. PKC immunolabelling studies detected a significant increase in PKC levels in membrane fractions 3 h but not 1 h after injury. Thus PKC activation is transiently increased following TBI and may play an important role in pathophysiologic responses to TBI.