ALTERATIONS OF PROTEIN-KINASE-C IN RAT HIPPOCAMPUS FOLLOWING TRAUMATIC BRAIN INJURY

Calcium-dependent excitotoxic processes contribute significantly to pa thologic responses to traumatic brain injury (TBI). TBI causes neurona l depolarization and excessive excitatory neurotransmitter release, wh ich may lead to increases in intracellular calcium levels. However, re sponses of calcium-dependent enzymes such as protein kinase C (PKC) fo llowing TBI are poorly understood. Since PKC plays an important role i n signal transduction and maintenance of normal neuronal function, we investigated changes in PKC activity and protein levels following flui d 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 postin jury. There was no statistically significant change in PKC activity 5 min and 24 h after injury. PKC immunolabelling studies detected a sign ificant increase in PKC levels in membrane fractions 3 h but not 1 h a fter injury. Thus PKC activation is transiently increased following TB I and may play an important role in pathophysiologic responses to TBI.