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Diabetic encephalopathy is a complication of diabetes mellitus characterized by impaired cognitive functions. Protein kinase C (PKC) isoforms are rarely reported on diabetic encephalopathy, although they have been believed to play crucial roles in other diabetic complications. In this study, streptozotocin- (STZ-) induced diabetic mice were found to exhibit learning and memory deficits in the Morris water maze test. Meanwhile, the expression of cPKC β II, nPKC ε , and cPKC γ  did not change in the hippocampus, cortex, and striatum at 2 and 8 weeks after STZ injection. The nPKC ε  translocation to the membrane, where it is activated, was not altered in the above brain regions at 2 and 8 weeks after STZ injection. Nevertheless, cPKC β II translocation to the membrane was significantly decreased in the cortex and hippocampus at 8 weeks after STZ injection. The translocation of cPKC γ  from the cytosol to the membrane was remarkably decreased in the hippocampus at 2 and 8 weeks and in the cortex and striatum at 8 weeks after STZ injection. In addition, deletion of cPKC γ  aggravated the impairment of spatial learning and memory. In conclusion, our results suggest that the decrease in the activity of cPKC β II and cPKC γ , especially cPKC γ , may play key roles in the pathogenesis of diabetic encephalopathy.

Identification of Protein Kinase C Isoforms Involved in Type 1 Diabetic Encephalopathy in Mice