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. Sustained changes in protein kinases content in PSD may cause persistent alteration in synaptic transmission. In the time course of reperfusion the activation state of key signaling molecules changes. Western blot analysis of phosphorylated forms of protein kinases revealed persistent activation of JNK, being limi- ted mostly to vulnerable CA1 region. On the contrary, activation of ERK, although observed transiently in both parts, was enhanced for a longer time in the abdominal, resistant part of hippocampus. More- over, the amount of active JNK linked with mitochondria was significantly increased and preceded neuronal death in CA1. In parallel, the amount of pro-survival Raf-1 kinase decreased in mitochondria and proapoptotic Bad protein content was increased. Concomitantly, transient ischemia evokes bipha- sic cytochrome c release from mitochondria. Cytochrom c in cytoplasm may be involved in the activa- tion of apoptosom, therefore cascade of caspases. Chasing a protein translocation in brain ischemia pathology this is a new research approach which might contribute to understand of the whole process and to search for a new points to prevent neuronal death.