Fatty Acids in Energy Metabolism of the Central Nervous System

Figure 4

Schematic representation of the mechanism for glutamate-induced glycolysis in astrocytes during physiological activation (from [93]). At glutamatergic synapses, presynaptically released glutamate depolarizes postsynaptic neurons by acting at specific receptor subtypes. The action of glutamate is terminated by an efficient glutamate uptake system located primarily in astrocytes. Glutamate is cotransported with Na⁺, resulting in an increase in the astrocytic sodium concentration leading to activation of the astrocyte Na⁺/K⁺-ATPase. Activation of the Na⁺/K⁺-ATPase stimulates glycolysis, that is, glucose consumption and lactate production. Lactate, once released by astrocytes, can be taken up by neurons and serves them as an adequate energy substrate. (Note: from further reading of the paper, it becomes clear that “PGK” should, in fact, be “PDH,” pyruvate dehydrogenase, which provides acetyl-CoA to the TCA cycle and further electrons to respiratory chain of mitochondria.)