The aim of the present study was to investigate, with extracellular recording and microiontophoretic techniques, the possibility that gamma-aminobutyric acid (GABA) is the transmitter substance in the pallido-subthalamic (GP-STN) pathway. Experiments were carried out in 94 rats, anesthetized with ketamine. Among the 236 recorded STN neurons, 85 were inhibited by GP stimulation. This inhibition lasted 10--20 msec (mean duration +/- S.E.M. 13.45 +/- 0.5 msec). Control stimulations located either in the internal GP or in the striatum never elicited the same type of response as they did in the STN. STN neurons were inhibited by microiontophoretically applied GABA or muscimol. Iontophoretically applied bicuculline or picrotoxin reversibly blocked the GP-evoked inhibition at doses which blocked the GABA inhibitory responses but not those produced by glycine. The results are consistent with the hypothesis that GABA is the transmitter releasted by the inhibitory pallido-subthalamic pathway, and are in agreement with recent biochemical data. Nevertheless, on a few cells, strychnine blocked the GP-induced inhibition. This results is discussed in relation to the specificty of GABA and glycine antagonists.