Facing the lack of anti-phase oscillation in the parafascicular nucleus after dopamine depletion.

There is a large body of literature establishing that excessive neuronal synchronization and a shift in firing pattern within the cortico-basal ganglia circuit is implicated in Parkinson's disease (PD), yet a causal link between abnormal network oscillation and specific deficits in PD is lacking. It is proposed that enhanced (inhibitory) synchronous basal ganglia output could trigger anti-phase oscillatory activity in target thalamic nuclei, and entrain this abnormal synchronization within the cortico-basal ganglia loop through a reciprocal resonance mechanism. In a recent Experimental Neurology paper (2009), Parr-Brownlie et al. addressed this issue by assessing electrophysiological recordings in vivo in anesthetized control and dopamine-depleted rats induced by unilateral injection of 6-hydroxydopamine. Results from this study demonstrate that a shift in firing pattern in basal ganglia output neurons does not directly drive the distinctive oscillatory activity observed in the parafascicular nucleus after dopamine depletion. This commentary discusses possible mechanisms mediating the altered oscillatory activity found in the parafascicular nucleus after dopamine depletion and its link to the increased in-phase oscillations with synchronous firing in the subthalamic nucleus.