Effects of TRPM8 cation channels on pain mediator secretion in neuronal cells
TL;DR
It is thought that increasing the number of novel specific agonists and antagonists targeting TRPM8 gating would be useful therapeutic targets in manipulating molecular mechanisms of pain.
Abstract
Aims: Pain is triggered and continued by complex cellular and molecular mechanisms in both the peripheral and central nervous systems. To sense a painful stimulus, neuronal cells use different pain transduction pathways, including calcium signaling. Intracellular calcium concentration is regulated under the control of several cation channels’ activity, including transient receptor potential cation (TRP) channels superfamily members and one of them is the TRPM8 cation channel in humans. The aim of this study was to investigate the effects of the TRPM8 cation channel gating which is little known how they play a role in pain mechanisms at the molecular level.Methods: To identify the potential role of TRPM8 channel specific agonist and antagonist application on the expression or secretion of certain pain mediators such as CGRP, NKA, NOS1 and Substance P which are involved in nociceptive signal transduction using ELISA technique.Results: When the expression levels were evaluated, it was found that, except NKA three neuropeptide levels were altered by TRPM8 agonist and/or antagonist incubation.Conclusion: Based on these findings, it is thought that increasing the number of novel specific agonists and antagonists targeting TRPM8 gating would be useful therapeutic targets in manipulating molecular mechanisms of pain.