Evidence of a physiological role for use-dependent inactivation of NaV1.8 sodium channels.
Scroggs
Reese S
RS
Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, 855 Monroe Avenue, Memphis, TN 38163, USA. rscroggs@utmem.edu
D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D062559:NAV1.8 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins / Q000187:drug effects / Q000502:physiology*; D009619:Nociceptors / Q000502:physiology*; D051381:Rats; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D062559:NAV1.8 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins; C568319:Scn10a protein, rat; D015222:Sodium Channels; D013779:Tetrodotoxin