| First Author | Dong P | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 13869 |
| PubMed ID | 29066740 | Mgi Jnum | J:255399 |
| Mgi Id | MGI:6109420 | Doi | 10.1038/s41598-017-12770-0 |
| Citation | Dong P, et al. (2017) TRPC3 Is Dispensable for beta-Alanine Triggered Acute Itch. Sci Rep 7(1):13869 |
| abstractText | 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 beta-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 beta-alanine induced itch, and found that these mice exhibit normal responses to beta-alanine. At the cellular level, calcium influx triggered by beta-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 beta-alanine-induced acute itch. |
