Neuronal degeneration following transient global cerebral ischaemia develops from complex series of pathophysiological events that evolve in time and intracellular space. During both, the early and delayed, postischemic stages translocation of proteins to postsynaptic density (PSD) and mitochon- dria are probably associated with recovery or cell death in vulnerable brain regions. Early after the insult a significant increase in the amount of CamKII and PKC isoforms is observed in PSD.