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Related Experiment Videos

Patterned electrical activity modulates sodium channel expression in sensory neurons.

Joshua P Klein1, Elisabetta A Tendi, Sulayman D Dib-Hajj

  • 1Department of Neurology and PVA/EPVA Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA. stephen.waxman@yale.edu

Journal of Neuroscience Research
|September 30, 2003
PubMed
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Neuronal activity levels directly impact sodium channel gene expression in dorsal root ganglion neurons. Electrical stimulation down-regulates Nav1.8 and Nav1.9, independent of nerve growth factor, suggesting a novel mechanism for neuropathic pain development.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Peripheral nerve injury alters sodium channel gene expression in dorsal root ganglion (DRG) neurons.
  • This alteration may contribute to neuropathic pain through neuronal hyperexcitability and ectopic discharge.
  • The precise mechanisms driving these expression changes remain unclear, with neurotrophic factors implicated but not fully understood.

Purpose of the Study:

  • To investigate if changes in intrinsic neuronal activity alone can alter sodium channel gene expression.
  • To examine the effect of electrical stimulation on Nav1.3, Nav1.8, and Nav1.9 expression in cultured sensory neurons.
  • To determine if this effect is independent of nerve growth factor (NGF) availability.

Main Methods:

  • Cultured embryonic mouse sensory neurons were subjected to electrical stimulation.

Related Experiment Videos

  • Quantitative polymerase chain reaction (qPCR) was used to measure mRNA levels.
  • Immunocytochemistry was employed to assess protein levels.
  • Experiments were conducted under conditions where nerve growth factor (NGF) was not limiting.

    • Main Results:

    • Electrical stimulation did not significantly alter Nav1.3 expression.
    • A significant, activity-dependent down-regulation of Nav1.8 and Nav1.9 mRNA and protein levels was observed following stimulation.
    • These findings indicate a mechanism independent of NGF withdrawal.

    Conclusions:

    • Neuronal activity levels can modulate sodium channel gene expression in a subtype-specific manner.
    • Altered neuronal activity, independent of NGF, can down-regulate Nav1.8 and Nav1.9 expression.
    • This provides new insights into the molecular mechanisms underlying neuropathic pain.