With regard to the behaviour of striatal D-2 receptors it was possible to divide parkinsonian patients into two subgroups, because either an increase or a decrease in the number of D-2 receptors was found. Dyskinesias, daily fluctuations in performance, and psychotic episodes together with neuroleptic medication, were associated with an increase in the number of striatal D-2 receptors. Clinically, the patients with a decreased number of striatal D-2 receptors were more disabled and had lost the beneficial response to levodopa. In agreement with post-mortem brain studies, increased responses of prolactin secretion to TRH in vivo also suggested a decreased D-2 receptor function in parkinsonian patients with recent onset and supersensitivity in patients with on-off phenomena. D-3 receptor binding sites had decreased in the parkinsonian striatum. In contrast to D-2 receptors, the D-3 sites seem to be less sensitive to treatment with neuroleptic drugs. Changes in the binding of 3H-enkephalins indicated that there is a supersensitivity of a population of enkephalin receptors (delta) in the striatum and limbic system. Treatment with levodopa did not have any significant effect on the binding of 3H-enkephalins. The binding of 3H-naloxone decreased in the parkinsonian caudate nucleus, suggesting that a population of opiate receptors (mu) is located on the dopamine nerve terminals in the striatum. Thus there are multiple neuronal disturbances in the parkinsonian brain, although those of nigrostriatal dopamine neurons seem to be greater and more closely related to the parkinsonian clinical features and to treatment responses.