Alterations of Protein Kinase C in Rat Hippocampus Following Traumatic Brain Injury

Keyi Yang, William C. Taft, C. Edward Dixon, Carlo A. Todaro, Robert K Yu, Ronald L. Hayes

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)287-295
Number of pages9
JournalJournal of Neurotrauma
Volume10
Issue number3
DOIs
StatePublished - Jan 1 1993
Externally publishedYes

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ASJC Scopus subject areas

  • Clinical Neurology

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