Because of new data, anatomical and functional models of the basal gan
glia in normal and pathological conditions (e.g. Parkinson's and Hunti
ngton's diseases) have recently come under greater scrutiny. An update
of-these models is clearly timely, taking into consideration not only
changes in neuronal discharge rates, but also changes in the patterni
ng and synchronization of neuronal discharge, the role of extrastriata
l dopamine, and expanded intrinsic and input/output connections of the
se nuclei.