Abstract
The synchronized beta-band oscillations in the basal ganglia-cortical networks in Parkinson's disease (PD) may be responsible for PD motor symptoms or an epiphenomenon of dopamine loss. We investigated the causal role of beta-band activity in PD motor symptoms by testing the effects of beta-frequency subthalamic nucleus deep-brain stimulation (STN DBS) on the blink reflex excitability, amplitude, and plasticity in normal rats. Delivering 16Hz STN DBS produced the same increase in blink reflex excitability and impairment in blink reflex plasticity in normal rats as occurs in rats with 6-hydroxydopamine lesions and patients with PD. These deficits were not an artifact of STN DBS because, when these normal rats received 130Hz STN DBS, their blink characteristics were the same as without STN DBS. To demonstrate that the blink reflex disturbances with 16Hz STN DBS were frequency specific, we tested the same rats with 7Hz STN DBS, a theta-band frequency typical of dystonia. In contrast to beta stimulation, 7Hz STN DBS exaggerated the blink reflex plasticity as occurs in focal dystonia. Thus, without destroying dopamine neurons or blocking dopamine receptors, frequency-specific STN DBS can be used to create PD-like or dystonic-like symptoms in a normal rat.
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