Elucidation of molecular mechanisms of pathophysiological pain via nociceptive channels and establishment of pain-evaluating system

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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.