Na V 1.8/Na V 1.9 double deletion mildly affects acute pain responses in mice.

ABSTRACT:

Abstract

The 2 tetrodotoxin-resistant (TTXr) voltage-gated sodium channel subtypes Na V 1.8 and Na V 1.9 are important for peripheral pain signaling. As determinants of sensory neuron excitability, they are essential for the initial transduction of sensory stimuli, the electrogenesis of the action potential, and the release of neurotransmitters from sensory neuron terminals. Na V 1.8 and Na V 1.9, which are encoded by SCN10A and SCN11A , respectively, are predominantly expressed in pain-sensitive (nociceptive) neurons localized in the dorsal root ganglia (DRG) along the spinal cord and in the trigeminal ganglia. Mutations in these genes cause various pain disorders in humans. Gain-of-function missense variants in SCN10A result in small fiber neuropathy, while distinct SCN11A mutati

SUBMITTER: Alves-Simoes M 

PROVIDER: S-EPMC11921451 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature