Neuronal firing patterns outweigh circuitry oscillations in parkinsonian motor control

摘要: Neuronal oscillations at beta frequencies (20-50 Hz) in the cortico-basal ganglia circuits have long been leading theory for bradykinesia, slow movements that are cardinal symptoms Parkinson's disease (PD). The oscillation helped to drive a frequency-based design development of deep brain stimulation therapy PD. However, contrast this theory, here we found bradykinesia can be completely dissociated from rodent models. Instead, observed is causatively regulated by burst-firing pattern subthalamic nucleus (STN) feed-forward, or efferent-only, mechanism. Furthermore, STN and two independent mechanisms different NMDA receptors STN. Our results shift understanding pathophysiology an interactive oscillatory toward feed-forward mechanism coded firing patterns. This distinct may improve fundamental concepts motor control enable more selective targeting bradykinesia-specific PD therapy.