Use dependence of peripheral nociceptive conduction in the absence of tetrodotoxin‐resistant sodium channel subtypes

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp7299-list-0001">This study examines conduction in peripheral nerves and its use dependence in tetrodotoxin‐resistant (TTXr) sodium channel (Nav1.8, Nav1.9) knockout and wildtype animals.We observed use‐dependent decreases of single fibre and compound action potential amplitude in peripheral mouse C‐fibres (wildtype). This matches the previously published hypothesis that increased Na/K‐pump activity is not the underlying mechanism for use‐dependent changes of neural conduction.Knocking out TTXr sodium channels influences use‐dependent changes of conductive properties (action potential amplitude, latency, conduction safety) in the order Nav1.8 KO > Nav1.9KO > wildtype.This is most likely explained by different subsets of presumably (relatively) Nav1.7‐rich conducting fibres in knockout animals as compared to wildtypes, in combination with reduced per‐pulse sodium influx.