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Changes in protein kinase C (PKC) were compared in primary cortical neurons exposed to glutamate and in the CA-1 hippocampal region of rats subjected to transient cerebral ischaemia. After a 15-min exposure of cortical neurons to excitotoxic levels of glutamate, a 50-60% loss of membrane PKC activity but only about a 20% loss in the amount of enzyme was observed, suggesting that in addition to enzyme loss other mechanisms also contributed to the overall loss of membrane PKC activity. Glutamate induced a 25-40% decrease in immunodetectable levels of PKC alpha, beta, gamma, and lambda but no detectable changes in PCK epsilon and zeta. The loss of PKC activity coincided with a shift in electrophoretic mobility of PKC gamma, epsilon, and lambda, but not of PKC alpha, beta, or zeta, suggesting post-translational modification of some PKC isoforms. By comparison, in rats subjected to transient (15-min) global ischaemia, a similar 50-60% decrease in membrane PKC activity, a 20-25% loss in the amount of PKC, and a shift in PKC mobility were observed in CA-1 neurons 6 h post-reperfusion. In both the in vivo and the in vitro "ischaemic" models, administration of the AMPA receptor antagonist NBQX prevented the loss of PKC activity. These results indicate that the loss of PKC observed in in vivo ischaemia is likely to be due to excitotoxic damage and that this event can be closely mirrored in primary neuronal cultures damaged by glutamate.


Journal article


Cell Signal

Publication Date





291 - 295


Animals, Brain Ischemia, Cells, Cultured, Cerebral Cortex, Enzyme Induction, Excitatory Amino Acid Agonists, Glutamic Acid, Male, Neurons, Protein Kinase C, Rats, Rats, Wistar