Figure 10.

Schematic diagram representing action of εPKC on synaptosomal mitochondria after IPC. Our results suggest that IPC results in the redistribution of εPKC to crucial neuroprotective targets such as synaptic mitochondria. The levels of εPKC in synaptosomes isolated from hippocampus of ischemic preconditioned animals are higher compared with sham-operated animals at 48 h of reperfusion. We observed that activation of εPKC leads to increased rate of mitochondrial electron transport chain activity by modulating phosphorylation status of mitochondrial electron transport chain complexes. We also observed that activation of εPKC results in lower reactive oxygen species (H₂O₂) production and a moderate increase in mitochondrial membrane potential. Synaptosomal mitochondria are less susceptible to in vitro ischemia when εPKC activation was induced.