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Author Notes:

Corresponding Author: Dieter Jaeger, Department of Biology, Emory University 1510 Clifton Rd. NE, Atlanta, GA, 30322 404-727-8139; djaeger@emory.edu


Research Funding:

This work was supported by NINDS grant 5R01-NS039852 to D. Jaeger and F32 NS051020 to J.R. Edgerton.


  • globus pallidus
  • basal ganglia
  • sodium channel
  • synaptic
  • dendritic spike
  • oscillation
  • synchrony
  • model
  • Parkinson's disease

Dendritic sodium channels promote active decorrelation and reduce phase locking to parkinsonian input oscillations in model globus pallidus neurons


Journal Title:

Journal of Neuroscience Nursing


Volume 31, Number 30


, Pages 10919-10936

Type of Work:

Article | Post-print: After Peer Review


Correlated firing among populations of neurons is present throughout the brain and is often rhythmic in nature, observable as an oscillatory fluctuation in the local field potential. Although rhythmic population activity is believed to be critical for normal function in many brain areas, synchronized neural oscillations are associated with disease states in other cases. In the globus pallidus (GP in rodents, homolog of the primate GPe), pairs of neurons generally have uncorrelated firing in normal animals despite an anatomical organization suggesting that they should receive substantial common input. By contrast, correlated and rhythmic GP firing is observed in animal models of Parkinson's disease (PD). Based in part on these findings it has been proposed that an important part of basal ganglia function is active decorrelation, whereby redundant information is compressed. Mechanisms that implement active decorrelation, and changes that cause it to fail in PD, are subjects of great interest. Rat GP neurons express fast, transient voltage-dependent sodium channels (NaF channels) in their dendrites, with the expression level being highest near asymmetric synapses. We recently showed that the dendritic NaF density strongly influences the responsiveness of model GP neurons to synchronous excitatory inputs. In the present study we use rat GP neuron models to show that dendritic NaF channel expression is a potential cellular mechanism of active decorrelation. We further show that model neurons with lower dendritic NaF channel expression have a greater tendency to phase lock with oscillatory synaptic input patterns like those observed in PD.

Copyright information:

© 2011 the authors

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