Metabolic studies of gamma‐aminobutyric acid

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Abstract
The nature of the relationship between cellular oxidations and the metabolism of gamma-aminobutyric acid (GABA) and glutamic acid in mouse brain tissue was investigated. GABA is formed in brain tissue from glutamic acid by the action of glutamic acid decarboxylase (GAD). GABA transaminase (GABA-T) found in brain, other tissues and in microorganisms, catalyzes the transamination of GABA with [alpha] -ketoglutarate ([alpha]KG). Since [alpha]KG, glutamic acid, GAD, GABA and GABA-T are all found in the central nervous system, there exists the possibility of a shunt around the [alpha]-KG oxidase system by which [alpha]-KG could be withdrawn as glutamic acid by the donation of the amino group of GABA, and the carbon chain of GABA could enter the tricarboxylic acid cycle at the succinate level. Data consistent with this theory were obtained in experiments using GABA-1-C14 with rats and mice and with minces of mouse brain. An assay procedure for the measurement of GABA-T activity was developed. Other data indicate that GAD requires pyridoxal phosphate as a coenzyme. This can be synthesized in brain from adenosine triphosphate and pyridoxal. These and other data are briefly discussed in reference to the spread of excitatory impulses in the nervous system.