We employ electrophysiological and computational methods to show that the heat nociception deficit in Fhf2 knockout mice can be explained by the combined effects of elevated temperature and FHF2 deficiency on the fast inactivation gating of Na v 1.7 and tetrodotoxin-resistant sodium channels expressed in dorsal root ganglion C-fibers.
Region(s) or Organism(s): Mouse
Cell Type(s): Dorsal Root Ganglion (DRG) cell
Currents: I Sodium; I Calcium; I h; I Potassium
Model Concept(s): Nociception; Action Potentials; Temperature
Implementer(s): Goldfarb, Mitchell goldfarb at genectr.hunter.cuny.edu]
References:
Marra C, Hartke TV, Ringkamp M, Goldfarb M. (2023). Enhanced sodium channel inactivation by temperature and FHF2 deficiency blocks heat nociception Pain. 164 [PubMed]