Abstract
The effect of activation and inhibition of protein kinase C (PKC) on the capacity of neurons to resist subsequent ischemic and ischemia-reperfusion-induced cell injury, was studied in a model of primary rat neuronal cultures, subjected to chemical ischemia. Activation of PKC by 1,2 dioctanoyl-rac-glycerol (DOG; 1 μM), or phorbol 12-myristate 13-acetate (PMA; 1 μM), as well as inhibition of the enzyme by chelerythrine (10 μM), or by calphostin C (0.2 μM), 10 min before the ischemic insult, resulted in acquisition of resistance against the two insults. The length of the `time window of protection' induced by exposure to DOG and to chelerythrine was studied and found to last for several days. The results demonstrate an apparently `paradoxical' phenomenon, in which both activation and inhibition of PKC in the same tissue induce protection. This may be explained by differential activation of various PKC isoforms.
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