TRPC3 Is Dispensable for β-Alanine Triggered Acute Itch
TRPC3 Is Dispensable for β-Alanine Triggered Acute Itch
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DOI：
10.1038/s41598-017-12770-0
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发表时间：
2017-10-24
影响因子：
4.6
通讯作者：
Luo, Wenqin
中科院分区：
文献类型：
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作者：
Dong, Peter;Guo, Changxiong;Luo, Wenqin
瘙痒（发痒）刺激的检测由初级感觉神经元表达的多种受体和通道介导。G蛋白偶联受体（GPCR）MRGPRD由小鼠非肽能伤害感受器的子集选择性表达，并作为瘙痒诱导化学物质β-丙氨酸的分子受体发挥作用。然而，负责产生MRGPRD下游电信号的通道仍不清楚。在这里，我们发现，典型的TRP通道家族的成员，TRPC 3，在MRGPRD+非肽能伤害感受器中高度表达，提高了TRPC 3是否作为MRGPRD信号通路的下游通道的可能性。我们测试了TrpC 3缺失小鼠的β-丙氨酸诱导的瘙痒，发现这些小鼠对β-丙氨酸表现出正常的反应。在细胞水平上，与野生型相比，由β-丙氨酸触发的钙内流在TrpC 3缺失小鼠的培养DRG神经元中也没有变化。总之，我们的结果表明，小鼠TrpC 3是β-丙氨酸诱导的急性瘙痒的抑制剂。
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.