The study investigates the relationship between cerebral glucose metabolism and glutamatergic neuronal function using 13C NMR spectroscopy to measure the rates of the tricarboxylic acid (TCA) cycle and glutamine (Gln) synthesis in the rat cortex in vivo. The researchers calculated the rates of oxidative glucose metabolism and glutamate-neurotransmitter cycling between neurons and astrocytes, providing a quantitative measure of glutamatergic neuronal activity. By measuring these rates over a range of synaptic activity, they found a stoichiometry between oxidative glucose metabolism and glutamate-neurotransmitter cycling close to 1:1, indicating that most cortical energy production supports functional (synaptic) glutamatergic neuronal activity. This suggests that brain activation studies mapping cortical oxidative glucose metabolism can provide a quantitative measure of synaptic glutamate release. The findings support a model of coupling between astrocytic glucose consumption and glutamatergic neuronal activity, where the majority of glycolytic glucose consumption in the brain occurs in glial cells, which export lactate to neurons for oxidative metabolism. The study also discusses the potential contribution of GABAergic neurotransmitter cycling to the overall rate of Gln synthesis but concludes that it does not significantly alter the observed stoichiometry.The study investigates the relationship between cerebral glucose metabolism and glutamatergic neuronal function using 13C NMR spectroscopy to measure the rates of the tricarboxylic acid (TCA) cycle and glutamine (Gln) synthesis in the rat cortex in vivo. The researchers calculated the rates of oxidative glucose metabolism and glutamate-neurotransmitter cycling between neurons and astrocytes, providing a quantitative measure of glutamatergic neuronal activity. By measuring these rates over a range of synaptic activity, they found a stoichiometry between oxidative glucose metabolism and glutamate-neurotransmitter cycling close to 1:1, indicating that most cortical energy production supports functional (synaptic) glutamatergic neuronal activity. This suggests that brain activation studies mapping cortical oxidative glucose metabolism can provide a quantitative measure of synaptic glutamate release. The findings support a model of coupling between astrocytic glucose consumption and glutamatergic neuronal activity, where the majority of glycolytic glucose consumption in the brain occurs in glial cells, which export lactate to neurons for oxidative metabolism. The study also discusses the potential contribution of GABAergic neurotransmitter cycling to the overall rate of Gln synthesis but concludes that it does not significantly alter the observed stoichiometry.