Regional rates of brain glucose utilization (rCMRglc) and glucose influx (rJin), along with regional brain tissue glucose concentrations, were measured in chronically hyperglycemic diabetic (CHD) rats following acute glycemic normalization. These results were compared to those obtained in nondiabetic normoglycemic controls. The diabetic rats were evaluated at 6-8 weeks following i.p. streptozotocin injection. All rats were N2O (70%) sedated, paralyzed, and artificially ventilated for study. Acutely normoglycemic (plasma glucose = 8.5 mumol/ml), demonstrated significantly higher (p less than 0.05) rCMRglc and rJin values in 8 of the 11 regions analyzed. Tissue/plasma glucose concentration ratios were significantly greater than control in 9 of 11 regions. Prior to acute glycemic normalization, rCMRglc values in CHD rats were either unchanged or moderately lower than control. These findings indicate that no blood-brain barrier glucose transport repression is present in CHD rats. In fact, the results suggest an increased transport capacity. The increased rCMRglc observed in the acutely normalized CHD rats may be a manifestation of the "hypoglycemic symptoms" observed in chronically hyperglycemic patients following acute glycemic reductions to the normal range. The present results imply that these symptoms are not related to the presence of a relative cerebral glucopenia, as others have suggested.