Carbon dioxide fixation in the brain / Soll Berl, Genkichiro Takagaki, Donald D Clarke, and Heinrich Waelsch From the New York Psychiatric Institute and the Colleg eof Physicians and Surgeons, Columbia University, New York, New York

Carbon dioxide fixation in brain was studied in cats to which NaHC14O3, with and without ammonia, was administered by intracarotid infusion. Glutamic and aspartic acids, glutamine, glutathione, and γ-aminobutyric acid were isolated from blood, brain, and liver, and their specific activities were determined. The data indicate a significant incorporation of CO2 into the amino acids of the cerebral cortex, presumably by way of the citric acid cycle. Without simultaneous ammonia infusion, the specific activity of aspartic acid is 3 times that of glutamine, whereas in the presence of ammonia the ratios of specific activity of both compounds are closer to unity or reversed. The data suggest that in the presence of ammonia the oxaloacetic acid is channeled into glutamine formation. γ-Aminobutyric acid isolated from the tissue, as well as that obtained after decarboxylation of glutamic acid or glutamine, has less than 5% of the counts of the precursor. These findings give additional support to the assumption that the operation of a CO2 fixation mechanism in brain is similar to that in liver. Additional data on the compartmentation of glutamic acid and glutamine synthesis are presented. The significance of the findings for an interpretation of ammonia metabolism in brain is pointed ou