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Related Experiment Videos

Sodium channels and pain.

S G Waxman1, S Dib-Hajj, T R Cummins

  • 1Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA.

Proceedings of the National Academy of Sciences of the United States of America
|July 8, 1999
PubMed
Summary
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Primary sensory neuron hyperexcitability, linked to pain, involves dynamic changes in sodium channel gene expression after injury. This plasticity in sodium channels in dorsal root ganglion neurons contributes to abnormal firing and pain pathophysiology.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Hyperexcitability of primary sensory neurons is linked to pain.
  • Molecular mechanisms of neuronal hyperexcitability after injury are not fully understood.
  • Axon injury can alter neuronal excitability, potentially via sodium channel changes.

Purpose of the Study:

  • Investigate the specific sodium channels responsible for primary sensory neuron hyperexcitability post-injury.
  • Understand the molecular basis of altered neuronal excitability and pain.

Main Methods:

  • Ensemble of molecular, electrophysiological, and pharmacological techniques.
  • Cloning and sequencing of dorsal root ganglion (DRG) neuron-specific sodium channels.
  • Analysis of sodium channel gene expression changes after axon injury.

Related Experiment Videos

Main Results:

  • Multiple sodium channels with distinct properties exist in small DRG neurons.
  • Axon injury causes significant changes in sodium channel gene expression (up- and down-regulation).
  • A previously silent sodium channel gene becomes up-regulated after injury.

Conclusions:

  • Sodium channel expression in DRG neurons is plastic and dynamically regulated after injury.
  • These changes in gene expression lead to altered electrophysiological properties, promoting abnormal neuronal firing.
  • Dynamic sodium channel expression in primary sensory neurons plays a key role in pain pathophysiology.