Experimentally induced changes in the concentration of GABA were studied in regions where GABA is present, predominantly in nerve terminals (substantia nigra, pituitary gland) or outside nerve terminals (corpus callosum). Some other regions (cerebellum, cuneate nucleus, corpus striatum, hippocampus) were included where the cellular localization of GABA is less certain. The post mortem increase in GABA was about equal percentage-wise in all regions indicating that it occurs in all locations where GABA is present. The increase in GABA following the GABA alpha-ketoglutaric acid aminotransferase inhibitor gamma-acetylenic GABA was much greater in the corpus callosum than in the other regions indicating that this enzyme is more important for the GABA present outside than inside the GABA nerve terminals. The glutamic acid decarboxylase inhibitor 4-deoxypyridoxine decreased the endogenous concentration of GABA and it inhibited the increase in GABA induced by gamma-acetylenic GABA in the substantia nigra and in the pituitary gland, but not in the corpus callosum, indicating that this compound inhibits the decarboxylase mainly in the GABA nerve terminals.