Energetics of functional activation in neural tissues

Glucose utilization (1CMR(glc)) increases linearly with spike frequency in neuropil but not perikarya of functionally activated neural tissues. Electr ical stimulation, increased extracellular [K+] ([K+](alpha)), or opening of Na+ channels with veratridine stimulates 1CMR(glc) in neural tissues; thes e increases are blocked by ouabain, an inhibitor of Na+,K-divided by-ATPase . Stimulating Na+,K-divided by-ATPase activity to restore ionic gradients d egraded by enhanced spike activity appears to trigger these increases in 1C MR(glc). Cultured neurons behave similarly. Astrocytic processes that envel op synapses in neuropil probably contribute to the increased 1CMR(glc). 1CM R(glc) in cultured astroglia is unaffected by elevated [K+](alpha) but is s timulated by increased intracellular [Na+] ([Na+](i)), and this stimulation is blocked by ouabain or tetrodotoxin. L-Glutamate also stimulates 1CMR(gl c), in astroglia. This effect is unaffected by inhibitors of NMDA or non-NM DA receptors, blocked by ouabain, and absent in Na+ -free medium; it appear s to be mediated by increased [Na+](i), due to combined uptake of Na+ with glutamate via Na+/glutamate co-transporters.