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Voltage-gated sodium channels (VGSCs), specifically Nav1.7, Nav1.8, and Nav1.9, are essential for pain signaling in nociceptors. They contribute to action potential generation and modulation of neuronal excitability. Mutations can cause altered pain sensitivity, and they are major targets for novel analgesics. These channels are dynamically regulated following nerve injury or inflammation and upregulation can contribute to hyperexcitability seen in chronic pain states.
Block voltage-gated sodium channels, preventing sodium influx and action potential generation/propagation.
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