Energetics of Functional Activation in Neural Tissues

Glucose utilization (lCMR_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 lCMR_glc. Cultured neurons behave similarly. Astrocytic processes that envelop synapses in neuropil probably contribute to the increased lCMR_glc. lCMR_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 lCMR_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.