A model of basal ganglia functioning proposed a few years ago suggests that increased and decreased activity in basal ganglia output to the thalamus underlies akinesia, as seen in Parkinson's disease, and dyskinetic movements as seen in Huntington's disease or after treatment with L-dopa and neuroleptics, respectively. Although the basic features of this model have stood the test of time, patterns of electrophysiological activity and changes in indices of GABA-dependent transmission in the external pallidum lead to a reconsideration of the mechanisms responsible for these changes in output activity.