EN
(1) We favour a hypothesis that the delayed <neuronal injury> in <hippocampus> is iniated 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>.