Behavior of ion channels controlled by electric potential difference and of Toll-type receptors in neuropathic pain pathophysiology

Abstract

BACKGROUND AND OBJECTIVES: Neuropathic pain is a severe and refrac-tory medical condition, for which only partially effective treatments are currently available. Recent experimental data on the role of voltage-gated ion channels, particularly sodium and potassium channels, have been described. In this brief review, we aimed at addressing the role of sodium and potassium channels in the pathophysiology of neuropathic pain and recent evidences about their role as a new therapeutic target in painful conditions. CONTENTS: Pharmacological and biophysical studies have shown that voltage-gated sodium channels, particularly Na v 1.3, Na v 1.7, Na v 1.8, and Na v 1.9 isoforms are important in the pathophysiology of neuropathic pain. Similarly, the involvement of voltage-gated potassium channels, especially K V 1 and K V 7 isoforms, has been clearly shown in the establishment of chronic painful conditions. Recent evidences that ion sodium and potassium channels dysfunction is involved in the development of chronic painful conditions corroborate the possibility of pharmacologically modulate them as new therapeutic strategies. CONCLUSION: Recent evidences suggest that selective sodium channel block-ers and potassium channels activating of modulating drugs are important and promising targets in the search for new options to treat neuropathic pain.