Short- and long-term dopamine depletion causes enhanced beta oscillations in the cortico-basal ganglia loop of parkinsonian rats.

Abnormally enhanced beta oscillations have been found in deep brain recordings from human Parkinson's disease (PD) patients and in animal models of PD. Recent correlative evidence suggests that beta oscillations are related to disease-specific symptoms such as akinesia and rigidity. However, this hypothesis has also been repeatedly questioned by studies showing no changes in beta power in animal models using an acute pharmacologic dopamine blockade. To further investigate the temporal dynamics of exaggerated beta synchrony in PD, we investigated the reserpine model, which is characterized by an acute and stable disruption of dopamine transmission, and compared it to the chronic progressive 6-hydroxydopamine (6-OHDA) model. Using simultaneous electrophysiological recordings in urethane anesthetized rats from the primary motor cortex, the subthalamic nucleus and the reticulate part of the substantia, we found evidence for enhanced beta oscillations in the basal ganglia of both animal models during the activated network state. In contrast to 6-OHDA, reserpine treated animals showed no involvement of primary motor cortex. Notably, beta coherence levels between primary motor cortex and basal ganglia nuclei were elevated in both models. Although both models exhibited elevated beta power and coherence levels, they differed substantially in respect to their mean peak frequency: while the 6-OHDA peak was located in the low beta range (17Hz), the reserpine peak was centered at higher beta frequencies (27Hz). Our results further support the hypothesis of an important pathophysiological relation between enhanced beta activity and akinesia in parkinsonism.