Neuronal firing patterns outweigh circuitry oscillations in parkinsonian motor control. Academic Article uri icon

Overview

abstract

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

publication date

  • October 31, 2016

Research

keywords

  • Biological Clocks
  • Neurons
  • Parkinson Disease
  • Subthalamic Nucleus

Identity

PubMed Central ID

  • PMC5127676

Scopus Document Identifier

  • 85002634339

Digital Object Identifier (DOI)

  • 10.1056/NEJMoa1205158

PubMed ID

  • 27797341

Additional Document Info

volume

  • 126

issue

  • 12