1. Medicine
  2. Neuroscience
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Parkinson’s Disease: Debunking an old theory

  1. Teresa Spix
  2. Aryn Gittis  Is a corresponding author
  1. Department of Biological Sciences, Carnegie Mellon University, United States
  2. Neuroscience Institute, Carnegie Mellon University, United States
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Cite this article as: eLife 2020;9:e62694 doi: 10.7554/eLife.62694
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Figures

Investigating the origin of cellular features associated with Parkinson’s disease.

(A) Neurons in the striatum express the D1 and D2 receptors for the neurotransmitter dopamine. The rate model predicts that the loss of dopamine in Parkinson’s disease decreases the activity of cells expressing the D1 receptor, increases the activity of cells expressing the D2 receptor (left), and increases the oscillatory activity of both D1 and D2 expressing neurons (right). These changes in activity are thought to alter the direct (turquoise) and indirect (purple) signals that D1-neurons and D2-neurons send to other structures in the basal ganglia. It is thought that this causes downstream neurons in the output nuclei of the basal ganglia to fire faster, more synchronously and with more oscillations – the pathophysiology commonly found in patients with Parkinson’s disease. (B) Valsky et al. tested this model on human patients with Parkinson’s disease and could not find any evidence of neurons in the striatum changing their firing rates or patterns of activity. This suggests that the neurological features associated with Parkinson’s disease do not stem from the striatum (as predicted by the rate model) but instead may originate downstream from the striatum (highlighted in yellow), in other structures of the basal ganglia.

Image credit: Teresa Spix.

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