Involvement of protein kinase C in various cellular systems transducting ischemia evoked signal

Abstract

(1) We favour a hypothesis that the delayed neuronal injury in hippocampus is initiated by the increase of intracellular calcium concentration, activating transiently Ca-dependent protein kinase. (2) The secondary effects of the postischemic, short-lasting PKC translocation/activation could involve: an activation of cAMP signaling pathway; an activation of early response protein like ornitine decarboxylase.