Energetics of functional activation in neural tissues

Abstract

Glucose utilization (1CMR(glc)) increases linearly with spike frequency in neuropil but not perikarya of functionally activated neural tissues. Electrical stimulation, increased extracellular [K+] ([K+]0), or opening of Na+ channels with veratridine stimulates 1CMR(glc) in neural tissues; these increases are blocked by ouabain, an inhibitor of Na+,K+-ATPase. Stimulating Na+,K+-ATPase activity to restore ionic gradients degraded by enhanced spike activity appears to trigger these increases in 1CMR(glc). Cultured neurons behave similarly. Astrocytic processes that envelop synapses in neuropil probably contribute to the increased 1CMR(glc). 1CMR(glc) in cultured astroglia is unaffected by elevated [K+]0 but is stimulated by increased intracellular [Na+] ([Na+](i)), and this stimulation is blocked by ouabain or tetrodotoxin. L-Glutamate also stimulates 1CMR(glc) in astroglia. This effect is unaffected by inhibitors of NMDA or non-NMDA receptors, blocked by ouabain, and absent in Na+-free medium; it appears to be mediated by increased [Na+](i) due to combined uptake of Na+ with glutamate via Na+/glutamate co-transporters.