Abstract
Summary
In agreement with previously reported enzymatic studies, experiments with intracerebrally administered L-glutamic-U-C14 in intact mice showed that carbon chain of L-glutamic acid is a source of the carbon chain of GABA formed in brain and that thiosemicarbazide decreases the rate of conversion of cerebral glutamic acid to GABA. It was shown that carbon of GABA can enter the tricarboxylic acid cycle at the succinate level in intact rats in experiments with intraperitoneally administered GABA-1-C14 employing the isotope trapping technic. Experiments in which GABA-1-C14 was injected intracerebrally to mice, or incubated with minces of mouse brain, indicated that utilization of GABA in brain probably takes place by the same mechanism as in the whole animal. The results of present and past biochemical studies can be correlated with relevant physiological data.
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