The human NaV1.8 (SCN10A; NP_006505) and the β3 subunit (SCN3B; NP_060870) cDNA was cloned and transfected into CHO cells and then the functional properties of the NaV1.8/β3 channels validated by means of manual and automated patch-clamp, including QPatch™.
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NaV1.8 voltage-gated sodium channel, is characterized by its activation at more depolarized membrane potentials and relatively fast activation and inactivation kinetics. Unlike NaV1.9, NaV1.8 plays a key role in the generation and propagation of action potentials in nociceptive neurons, particularly under conditions of low temperature, making it especially relevant for peripheral pain signaling. NaV1.8 is resistant to tetrodotoxin (TTX) and is predominantly expressed in peripheral sensory neurons. The beta3 subunit modulates NaV1.8 channel properties by influencing its trafficking to the membrane and altering its kinetic behavior. The interaction between NaV1.8 α and ß3 is thought to contribute to neuronal excitability and may be involved in the development of chronic pain states. Given its involvement in nociceptive signaling, NaV1.8 represents a promising target for the development of novel analgesic therapies.