2013 Fiscal Year Final Research Report
Elucidation of molecular mechanisms of pathophysiological pain via nociceptive channels and establishment of pain-evaluating system
| Project/Area Number |
22380160
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Basic veterinary science/Basic zootechnical science
|
|---|
| Research Institution | Tottori University |
|---|
Principal Investigator |
OHTA Toshio 鳥取大学, 農学部, 教授 (20176895)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Kenji 鳥取大学, 農学部, 准教授 (00400143)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
IMAGAWA Toshiaki 北海道大学, 理学研究科, 准教授 (20142177)
|
|---|
| Project Period (FY) |
2010-04-01 – 2014-03-31
|
| Keywords | 薬理 |
|---|
| Research Abstract |
We cloned cDNA encoding nociceptive channels from amphibian and chicken and constructed expression vectors. We established nociception-evaluating system for elucidation of the pathophysiological significance of these receptors. Using this system, we found that the recognition sites for capsaicin, a pungent compound for TRPV1. Functional expression and characterizing of X. troplicalis TRPA1 revealed that amphibian TRPA1 showed heat sensitivity in contrast to homoeothermic homologues. By analyzing human and mouse TRPA1s, Cadmium, an environmental irritant and hydrogen sulfide, en endogenous inflammatory gasomessenger, could activate TRPA1 channel resulting in elicitation of acute pain. We identified amino acid residues regarding these chemical sensitivities by mutagenetic studies. These data suggest that nociceptive TRP channels are important molecule especially for inflammation-induced pathophysiological pain.
|
