Effects of glucose on calcium channels in neural cells.

Hyperglycemia has been reported to alter outcome following experimental and clinical cerebral ischemia, but the mechanisms involved are incompletely understood. Since glucose influences the function of dihydropyridine-sensitive, voltage-gated Ca2+ channels in some non-neural cells, and since cellular Ca2+ overload has been implicated in the pathogenesis of ischemic neuronal injury, we examined whether glucose regulates Ca2+ channel function in a cultured neural cell line. Physiologic concentrations of glucose had no effect on free intracellular Ca2+ levels in PC12 cells, but 4-fold elevation of glucose above physiologic levels reduced the dihydropyridine-sensitive, depolarization-induced increase in Ca2+. This effect would not account for exacerbation of ischemic brain injury by hyperglycemia, but may contribute to attenuation of ischemic injury by glucose in certain settings.