神经病理性疼痛
机械反应
痛觉超敏
医学
压电1
伤害
门控
神经科学
感觉系统
神经损伤
灵敏度(控制系统)
慢性疼痛
麻醉
瞬时受体电位通道
机制(生物学)
神经痛
药理学
电生理学
钠通道
伤害感受器
频道(广播)
钙通道
机械转化
离子通道
痛觉过敏
TRPV1型
作者
Abdella M. Habib,Shengnan Li,Chenjing Zhang,Mengyue Ji,Nancy Osorio,Virginie Pénalba,Jesús M. Torres,Samuel J. Gossage,Mehdi A. Rezai,Amy Geard,Ahad A. Rahim,Ahmed M. M. Mahmoud,Sonia Santana‐Varela,Jun Zhou,Jing Zhao,John N. Wood,Andrei L. Okorokov,Xuelong Zhou,James J. Cox,Bertrand Coste
标识
DOI:10.1073/pnas.2512426122
摘要
PIEZO channels are mechanical force sensors involved in various biological processes, including somatosensation. To date, only a few PIEZO-binding partners have been identified, including MyoD-family inhibitor proteins (MDFI and MDFIC). Here, we show that MDFIC2, a third member of the MDFI protein family with an as-yet-unknown function, is expressed in a subset of nociceptive sensory neurons. MDFIC2 modulates both PIEZO1 and PIEZO2 gating properties by slowing their kinetics and shifting mechanical sensitivity to higher forces. Interestingly, Mdfic2 is downregulated in mouse neuropathic pain models in which mechanical allodynia is a hallmark symptom. We found that intrathecal administration of adeno-associated virus vector encoding MDFIC2 cDNA reduces mechanical sensitivity and attenuates mechanical allodynia in the spared nerve injury neuropathic pain model. These findings demonstrate a mechanism for regulating mechanosensation and highlight a potential therapeutic route for treating mechanical allodynia.
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