GPi, GPe and putamen firing changes induced by apomorphine in parkinson's disease patients

Firing activity of GPi cells was recorded from six nuclei of three Parkinson's disease (PD) patients during neurosurgical procedure, before and after administration of repeated doses of apomorphine. GPi cells in PD patients display the spontaneous high frequency activity that was clearly decreased by apomorphine in a dose dependent manner similarly to that reported in monkey treated with MPTP. Repeated administration of apomorphine produced a clinical and electrophysiological evident desensitization. Differently, simultaneous recording from GPe (n=2) and putamen (n=1) cells did not show clear firing frequency modifications in both nuclei. However, GPe cells exibiting bursting activity in control condition, showed a tendency to change their pattern into regular firing. These findings suggest no direct relationship between uiji hyperacuvity and Gpe tiring frequency. Apomorphine doses causing dyskinesia produced involuntary movements before GPi cells decreased their frequency discharge, suggesting that GPi is not directly involved in the genesis of dyskinesia. Bipolar stimulation of putamen evoked an inhibitory (10-20 ms)-excitatory (30-50 ms) sequence in GPi cells, but not in the GPe and putamen recorded cells. The excitatory component was markedly decreased by apomorphine administrations. These findings suggest a strong relationship between GPi activity and parkinsonian clinical symptoms, while they tend to exclude that a GPe overinhibition is responsable for the GPi hyperactivity. If the poststimulus excitation observed in GPi cells is due to subthalamic driving, then apomorphine-induced decrease of this excitation suggests that GPi hyperactivity is produced by subthalamus through a pathwy not involving GPe.