Previous studies have shown that the level of total conventional protein kinase C (cPKC) membrane translocation (activation) was increased in brain of hypoxic preconditioned mice. In order to find out which isoform of cPKC may participate in the development of cerebral hypoxic preconditioning (HPC), we used Western bolt and immunohistochemistry to observe the effects of repetitive hypoxic exposure (H1-H6, n=6 for each group) on the level of cPKC isoform-specific protein expression and its membrane translocation in cortex and hippocampus of mice. We found that levels of cPKC βII and γ membrane translocation were increased significantly (p<0.05 versus normoxic H0 group, n=6) in response to repetitive hypoxic exposure (H1-H4) at early phase of hypoxic preconditioning, but no significant changes of cPKC α and βI membrane translocation while cPKC α, βI, βII and γ protein expression were found both in hippocampus and cortex. In addition, an extensive subcellular redistribution of cPKC βII and γ was detected by immunohistochemistry staining in cortex after repetitive hypoxic exposures (H3). However, a significant decrease in the expression of cPKC γ protein (p<0.05 versus H0 group) was found only in cortex of delayed hypoxic preconditioned mice (H5-6). These results suggested that the activation of cPKC βII and γ may be involved in the early phase of cerebral hypoxic preconditioning and the changes in cPKC γ protein expression may participate in the development of late phase of cerebral hypoxic preconditioning, as well as selective vulnerability to hypoxia both in cortex and hippocampus.