Abstract
Endocrinological research early recognized the importance ofintercellular interactions, initially in processes involved in lacta-tion, pubertal maturation, and regulation of the female ovariancycle and later in appetite regulation. The importance of gluta-matergicandGABAergicsignalingduringallof theseeventsisnowrealized. Reference (1) describes existing knowledge of the roleof amino acid neurotransmitters in the mechanism of neuronalactivation during appetite regulation and associated neuronal–astrocytic metabolic coupling mechanisms. Different responses inthese mechanisms are apparently originated in different feedingparadigms associated with appetite stimulation (1).Formation of transmitters glutamate and GABA requires pro-found interactions between neurons and astrocytes,as does resup-ply of released transmitters. Both of these amino acid transmittersare formed in brain from glucose in astrocytes (2, 3), but not inneurons, which lack the enzyme pyruvate carboxylase (PC). Themost recent progress in measurement of brain glucose transportand metabolism
Highlights
Formation of transmitters glutamate and GABA requires profound interactions between neurons and astrocytes, as does resupply of released transmitters. Both of these amino acid transmitters are formed in brain from glucose in astrocytes [2, 3], but not in neurons, which lack the enzyme pyruvate carboxylase (PC)
The most recent progress in measurement of brain glucose transport and metabolism in vivo and its importance for understanding of the glial role in glutamatergic and GABAergic neurons are reviewed in Ref. [4], which thoroughly describes different approaches to establish mathematical models of brain metabolism and apply them to obtain quantitative metabolic rates [4]
GABA formation is slightly more complex, since part of the glutamate – from which GABA is formed by decarboxylation – is treated but another major part is first partly metabolized via the tricarboxylic acid (TCA) cycle [2]
Summary
Formation of transmitters glutamate and GABA requires profound interactions between neurons and astrocytes, as does resupply of released transmitters. Both of these amino acid transmitters are formed in brain from glucose in astrocytes [2, 3], but not in neurons, which lack the enzyme pyruvate carboxylase (PC).
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