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Voltage-gated sodium channels and pain pathways
John N Wood1, James P Boorman, Kenji Okuse
1Molecular Nociception Group, Department of Biology, University College, Gower Street, London WC1E 6BT, UK. J.Wood@ucl.ac.uk
Journal of Neurobiology
|September 14, 2004
Summary
Local treatments with sodium channel blockers, like lidocaine, can reduce pain. Specific sodium channel types (Nav1.8, Nav1.9, Nav1.7, Nav1.3) are key to pain signaling, suggesting targeted blockers could be effective analgesics.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Pain perception relies on functional voltage-gated sodium channels in peripheral neurons.
- Specific sodium channel subtypes (Nav1.8, Nav1.9, Nav1.7, Nav1.3) are implicated in pain pathways.
Purpose of the Study:
- To investigate the role of specific voltage-gated sodium channels in acute, inflammatory, and neuropathic pain.
- To explore the potential of isotype-specific sodium channel blockers as analgesics.
Main Methods:
- Review of studies involving antisense and knock-out models.
- Analysis of pharmacological data from conotoxin studies.
Main Results:
- Nav1.8 and Nav1.9 channels are selectively expressed in damage-sensing neurons.
- Nav1.7 channels are found in sensory and sympathetic neurons.
- Nav1.3 channels are upregulated in neuropathic pain, increasing nerve excitability.
Conclusions:
- Voltage-gated sodium channels play a critical role in pain transmission.
- Targeting specific sodium channel isotypes offers a promising strategy for developing novel analgesics.