TY - JOUR
T1 - Differences in the acidic sensitivity of transient receptor potential vanilloid 1 (TRPV1) between chickens and mice
AU - Liang, Ruojun
AU - Kawabata, Yuko
AU - Kawabata, Fuminori
AU - Nishimura, Shotaro
AU - Tabata, Shoji
N1 - Funding Information:
We thank Prof. Makoto Tominaga and Dr. Shigeru Saito (Exploratory Research Center on Life and Living Systems) for providing the cTRPV1/pcDNA3.1 and Dr. Koji Shibasaki (Gunma University) for providing the EGFP/pCAGGS. We appreciate the technical assistance of The Research Support Center, Research Center for Human Disease Modeling, Kyushu University Graduate School of Medical Sciences. This study was supported by grants to F. Kawabata from the Kyushu University Interdisciplinary Programs in Education and Projects in Research Development (# 26703 ) and the Sugiyama Sangyo-Kagaku General Incorporated Foundation .
Funding Information:
We thank Prof. Makoto Tominaga and Dr. Shigeru Saito (Exploratory Research Center on Life and Living Systems) for providing the cTRPV1/pcDNA3.1 and Dr. Koji Shibasaki (Gunma University) for providing the EGFP/pCAGGS. We appreciate the technical assistance of The Research Support Center, Research Center for Human Disease Modeling, Kyushu University Graduate School of Medical Sciences. This study was supported by grants to F. Kawabata from the Kyushu University Interdisciplinary Programs in Education and Projects in Research Development (#26703) and the Sugiyama Sangyo-Kagaku General Incorporated Foundation.
Publisher Copyright:
© 2019 Elsevier Inc.
PY - 2019/7/23
Y1 - 2019/7/23
N2 - Chickens, one of the most important industrial animals, are a biological animal model. Here we focused on the transient receptor potential vanilloid 1 (TRPV1) to understand the pain system for acidic stimuli in chickens compared with mice. By using a whole-cell patch clamp system, we confirmed that acidic stimuli activate both chicken TRPV1 (cTRPV1) and mouse TRPV1 (mTRPV1), but the peak current of cTRPV1 is lower than that of mTRPV1, and it is difficult to desensitize cTRPV1 with an acidic stimulus compared to mTRPV1. Since the C-terminal of the calmodulin (CaM) binding site in TRPV1 was reported as one of the important structures for TRPV1 desensitization, we made chimeric cTRPV1 in which the CaM binding site of chicken is changed to that of mouse (cTRPV1-mCaM). We also compared the acidic responses of native chicken dorsal root ganglion (DRG) cells with that of mouse DRG cells. The TRPV1-mCaM results showed that the desensitization of mutant cTRPV1 was similar to that of mTRPV1, and that the basal activities of mutant cTRPV1 were significantly higher than those of cTRPV1. It was also difficult to desensitize the chicken DRG cells with an acidic stimulus, unlike the mouse DRG cells. These results suggest that there are differences in the pain transduction systems for acidic stimuli between chickens and mice that are caused by the dysfunction of the C-terminal CaM biding site of cTRPV1. These results imply that chickens repeatedly feel weak pain from an acidic stimulus, without desensitization.
AB - Chickens, one of the most important industrial animals, are a biological animal model. Here we focused on the transient receptor potential vanilloid 1 (TRPV1) to understand the pain system for acidic stimuli in chickens compared with mice. By using a whole-cell patch clamp system, we confirmed that acidic stimuli activate both chicken TRPV1 (cTRPV1) and mouse TRPV1 (mTRPV1), but the peak current of cTRPV1 is lower than that of mTRPV1, and it is difficult to desensitize cTRPV1 with an acidic stimulus compared to mTRPV1. Since the C-terminal of the calmodulin (CaM) binding site in TRPV1 was reported as one of the important structures for TRPV1 desensitization, we made chimeric cTRPV1 in which the CaM binding site of chicken is changed to that of mouse (cTRPV1-mCaM). We also compared the acidic responses of native chicken dorsal root ganglion (DRG) cells with that of mouse DRG cells. The TRPV1-mCaM results showed that the desensitization of mutant cTRPV1 was similar to that of mTRPV1, and that the basal activities of mutant cTRPV1 were significantly higher than those of cTRPV1. It was also difficult to desensitize the chicken DRG cells with an acidic stimulus, unlike the mouse DRG cells. These results suggest that there are differences in the pain transduction systems for acidic stimuli between chickens and mice that are caused by the dysfunction of the C-terminal CaM biding site of cTRPV1. These results imply that chickens repeatedly feel weak pain from an acidic stimulus, without desensitization.
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U2 - 10.1016/j.bbrc.2019.05.129
DO - 10.1016/j.bbrc.2019.05.129
M3 - Article
C2 - 31155288
AN - SCOPUS:85066279135
SN - 0006-291X
VL - 515
SP - 386
EP - 393
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -