[No authors listed]
Diabetic encephalopathy is a complication of diabetes mellitus characterized by impaired cognitive functions. Protein kinase C 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 and did not change in the hippocampus, cortex, and striatum at 2 and 8 weeks after STZ injection. The 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, translocation to the membrane was significantly decreased in the cortex and hippocampus at 8 weeks after STZ injection. The translocation of cduanyu1531γ 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 cduanyu1531γ aggravated the impairment of spatial learning and memory. In conclusion, our results suggest that the decrease in the activity of cduanyu1531βII and especially cduanyu1531γ, may play key roles in the pathogenesis of diabetic encephalopathy.
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