瘙痒是皮肤病的主要症状。动物和电生理学研究显示，瞬时受体电位通道V3亚型（TRPV3）在感觉中发挥重要作用，但它在瘙痒中的作用机制尚未明了。我们最近在国际上首次确定了一种严重的瘙痒和角化性疾病，Olmsted综合征，是由于TRPV3的功能增强型突变所导致。突变可引起通道的持续开放，使角质形成细胞中的钙离子浓度升高，凋亡加速，出现严重的角化。在患者的皮损中可发现大量的肥大细胞，其在瘙痒的产生中应具有关键作用。是由于肥大细胞表达了TRPV3，其功能增强而易于脱颗粒，还是角质形成细胞与肥大细胞间相互作用引起瘙痒，抑或兼而有之，是我们亟需阐明的问题。另外，TRPV3基因敲除小鼠的痒觉有何变化，其角质形成细胞和肥大细胞通过何种机制参与瘙痒的形成，也尚待明确。我们拟在以往的分子生物学和电生理学研究的基础上，在分子、细胞和动物水平揭示瞬时受体电位通道V3亚型在瘙痒中的作用，为瘙痒的治疗提供新思路。

Itch is a main symptom of skin disorders. Animal and electrophysiological studies revealed that, transient receptor potential channel subfamily V member 3 (TRPV3), plays important roles in sensation. But the functional mechanisms of TRPV3 in itch are largely unknown. Recently, we idnetified that, gain-of-function mutations of TRPV3 cause Olmsted syndrome, a genetic disease with severe itch and hyperkeratosis. Mutations caused channels constitutive opening, leading to elevated apoptosis of keratinocytes and consequent hyperkeratosis. Mast cell infiltrations are noted in the skin lesions, which should be a key factor for itch symptoms. Whether mast cells express TRPV3, which functional enhancements can lead mast cell easy to degranulate, or interactions between keratinocytes and mast cells cause itch? That is a problem need to be clarified. In addition, do the TRPV3 knockout mice have abnormal itch sensation? What are the roles of keratinocytes and mast cells in the itch sensation of these mice? It's also unknown. Based on our previous molecular biology and electrophysiology research, we intend to reveal the roles of TRPV3 in itch at the molecular, cellular and animal levels, and to provide new ideas for developing antipruritics.