TY - JOUR
T1 - TRPC3 Is Dispensable for β-Alanine Triggered Acute Itch
AU - Dong, Peter
AU - Guo, Changxiong
AU - Huang, Shengxiang
AU - Ma, Minghong
AU - Liu, Qin
AU - Luo, Wenqin
N1 - Funding Information:
We thank Drs. Barbara Miller and Craig Montell for sharing TrpC3 KO mice and anti-TRPC3 antibody with us. Additionally, we thank Tim O’Brien of the Penn Behavioral Neuroscience Core and Anna Vysochan for their help in planning the behavior experiments. We thank members of the Liu and Luo labs for reading the manuscript and providing helpful comments. Q.L. is supported by the National Institutes of Health (NIH) (1R01EY024704 and 1R01AI125743), and W.L. is supported by the NIH (R01NS083702 and R01NS094224) and the Klingenstein-Simons Fellowship Award in the Neurosciences.
Publisher Copyright:
© 2017 The Author(s).
PY - 2017/12/1
Y1 - 2017/12/1
N2 - The detection of pruritic (itchy) stimuli is mediated by a variety of receptors and channels expressed by primary sensory neurons. The G protein-coupled receptor (GPCR) MRGPRD is selectively expressed by a subset of mouse non-peptidergic nociceptors and functions as the molecular receptor for the itch-inducing chemical β-alanine. However, the channels responsible for generating electrical signals downstream of MRGPRD remain unclear. Here, we found that a member of the canonical TRP channel family, TRPC3, is highly expressed in MRGPRD+ non-peptidergic nociceptors, raising the possibility of whether TRPC3 functions as a downstream channel in the MRGPRD signaling pathway. We tested TrpC3 null mice for β-alanine induced itch, and found that these mice exhibit normal responses to β-alanine. At the cellular level, calcium influx triggered by β-alanine is also unchanged in cultured DRG neurons from TrpC3 null mice compared to wild type. Together, our results demonstrate that mouse TrpC3 is dispensable for β-alanine-induced acute itch.
AB - The detection of pruritic (itchy) stimuli is mediated by a variety of receptors and channels expressed by primary sensory neurons. The G protein-coupled receptor (GPCR) MRGPRD is selectively expressed by a subset of mouse non-peptidergic nociceptors and functions as the molecular receptor for the itch-inducing chemical β-alanine. However, the channels responsible for generating electrical signals downstream of MRGPRD remain unclear. Here, we found that a member of the canonical TRP channel family, TRPC3, is highly expressed in MRGPRD+ non-peptidergic nociceptors, raising the possibility of whether TRPC3 functions as a downstream channel in the MRGPRD signaling pathway. We tested TrpC3 null mice for β-alanine induced itch, and found that these mice exhibit normal responses to β-alanine. At the cellular level, calcium influx triggered by β-alanine is also unchanged in cultured DRG neurons from TrpC3 null mice compared to wild type. Together, our results demonstrate that mouse TrpC3 is dispensable for β-alanine-induced acute itch.
UR - http://www.scopus.com/inward/record.url?scp=85032173189&partnerID=8YFLogxK
U2 - 10.1038/s41598-017-12770-0
DO - 10.1038/s41598-017-12770-0
M3 - Article
C2 - 29066740
AN - SCOPUS:85032173189
SN - 2045-2322
VL - 7
JO - Scientific reports
JF - Scientific reports
IS - 1
M1 - 13869
ER -