After interuption of the striato-nigral pathway uptake of gamma-aminobutyric acid (GABA) in the substatia nigra decresaed with 7 days to a constant level 30-40% of the normal. Concomitantly glutamate decarbosylase (GAD) was reduced to 10%. Hence about two-thirds of the GABA uptake activity in substantia nigra are localised, to the alleged GABA-ergic nerve elements originating from corpus striatum. The lesion resistant part of the uptake is probably not localised in cell bodies or large processes, since it was the same in tissuse prisms as in whole homogenates and crude nerve ending fractions. It was also not influenced by aminoozyacetic acid, which would argue against a localisation in glia. Whereas GAD was recovered mainly in a "heavy" nerve ending fraction, a large proportion of the GABA uptake was situated in a "light" fraction. After hemisections, GABA uptake was reduced to a similar extent in both fractions. It is suggested that whereas GAD is concentrated in nerve terminals, a significant proportion of the GABA uptake may be localised in preterminal axon branches in the substantia nigra. GABA uptake in the dorsal part of the lateral vestibular nucleus was not reduced by interruption of the Purkinje axons from the cerebellar vermis whereas GAD was reduced 50%. This indicates that the reuptake mechanism is not concentrated in the Prukinje axon terminals. In the hippocampus neither GABA nor GAD were reduced by lesions of afferent nerve pathoways, in accordance with previous results showing that in this region GABA producing neurones are intrinsic. The order of ratiols of GABA uptake to particulate GAD activity in different regions was: hippocampus greater than cerebellar cortex greater than substantia nigra greater than dorsal part of lateral vestibular necleus approximately equal to nucleus interpositus. The ratio may relfect the degree of specific localisation of the GABA uptake mechanism to the GABA-ergic structures.