Regulation of Na+/myo-inositol cotransporter gene expression in hyperglycemic rat hippocampus

myo-Inositol is accumulated into cells by means of the Na+/myo-inositol cotransporter (SMIT), which is of interest because its activity is upregulated by hyperosmotic stress. We investigated the effects of hyperglycemia on the expression of SMIT mRNA mainly in rat hippocampus. In normal control rats, SMIT mRNA signals were predominantly located in the hippocampus, cerebellum and choroid plexus. Interestingly, massive induction in the hippocampus was observed on the acute stage of induced hyperglycemia in the CA3/CA4, the molecular layer of the dentate gyrus, and the hippocampal fissure. The perivascular cells along the hippocampal fissure also expressed prominent signals. In the cerebral cortex, heterogeneous induction was observed from layers 2 to 6. Furthermore, these changes immediately returned to baseline levels after normalization of glucose levels. These results suggest that regional specificity of permeability of the blood-brain barrier and/or cellular differences in sensitivity to hyperglycemic stress would exist in the brain.