article = {NNB-2018-2-101}
title = {Ion channels involved in spontaneous pain}
journal = {Neurology and Neurobiology}
year = {2018}
issn = {2613-7828}
doi = {http://dx.doi.org/10.31487/j.NNB.2018.02.001}
url = {https://www.sciencerepository.org/ion-channels-involved-in-spontaneous-pain_NNB-2-101 
author = {Hiroki  Toyoda,}
keywords = {ion channel, spontaneous pain, neuron}
abstract ={Pain is a distressing feeling that is often induced by damaging stimuli. The nerve injuries cause various
molecular changes in nociceptive primary afferent neurons that cause spontaneous pain. Furthermore, the
nerve trunk injury induces ectopic discharge, resulting in spontaneous pain. To date, accumulating evidence
suggests that ion channels which are responsible for neuronal excitability play key roles in generation of
spontaneous pain. It is believed that voltage-gated Na+
channels (VGSCs) and Ca2+ channels (VGCCs) are
the primary membrane proteins for causing spontaneous pain. However, it has been evident that various ion
channels including transient receptor potential (TRP) channels, hyperpolarization-activated cyclic
nucleotide–gated (HCN) channels and acid-sensing ion channels (ASICs) are associated with generation of
spontaneous pain. In the present review, I will describe the current knowledge on ion channels related to
spontaneous pain}