Abstract: Abstract: Objective To explore the role of cPKCgamma in hypoxic preconditioning (HPC) regulating hydrolysis and phosphorylation of collapsin response mediated protein 2 (CRMP2) in the ischemic cortex of mice. Methods Using our established HPC and middle cerebral artery occlusion (MCAO) BALB/c mouse models (male,18-22g), We applied Western blot, immunoprecipitation (IP) and immunohistochemisty to determine the effect of cPKCgamma activation on CRMP2 hydrolysis and phosphorylation, cPKCgamma-CRMP2 interaction and p-CRMP2 positive cells’ number in the peri-infarct region of MCAO mice. Results We found that HPC could inhibit both the decrease of p-CRMP2 level and increase of BDP in peri-infarct region of ischemic cortex. Pretreatment of cPKCgmma inhibitor Go6983 (6nM) could depress the HPC-induced inhibitory effect on CRMP2 dephosphorylation and hydrolysis in peri-infarct area of ischemic cortex; IP results showed that the activity of cPKCgamma could affect the interaction between cPKCgamma and CRMP2; in addition, the immunohistochemistry results also demonstrated the same effect of cPKCgamma on p-CRMP2 positive cells in peri-infarct region of ischemic cortex. Conclusion cPKCgamma was involved in the regulation of HPC on CRMP2 phosphorylation and hydrolysis in ischemic cortex of MCAO mice.

Key words: HPC, middle cerebral artery occlusion, cPKC?, CRMP2