GABA metabolism and cerebral protein synthesis.
Glutamate decarboxylase (GAD) activity and [14C)leucine incorporation into brain protein in vivo were measured in mice injected with L-glutamic acid-gamma-hydrazide and 60 min later with pyridoxal-5'-phosphate; this combined treatment produces a decrease in GAD activity and an increase in GABA levels. Under such conditions, protein synthesis was inhibited to the same extent as GAD activity. A parellelism between the decrease in GAD activity and that in protein synthesis was also observed in brain cortex slices treated with GAD inhibitors. This treatment did  not affect leucine incorporation into protein in liver slices. The results support the previously suggested hypothesis that a certain pool of GABA may have a role in the regulation of protein synthesis in brain, and further suggest that the synthesis of GABA may be more important in this respect than its total concentration.
D000613:Aminobutyrates / Q000378:metabolism*; D000625:Aminooxyacetic Acid / Q000494:pharmacology; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D005968:Glutamate Decarboxylase / Q000032:analysis; D005971:Glutamates / Q000378:metabolism; D006834:Hydrazines / Q000494:pharmacology; D066298:In Vitro Techniques; D007930:Leucine / Q000378:metabolism; D051379:Mice; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D010091:Oximes / Q000494:pharmacology; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D000613:Aminobutyrates; D005971:Glutamates; D006834:Hydrazines; D009419:Nerve Tissue Proteins; D010091:Oximes; D000625:Aminooxyacetic Acid; D005680:gamma-Aminobutyric Acid; D011732:Pyridoxal Phosphate; D005968:Glutamate Decarboxylase; D007930:Leucine; D001640:Bicuculline