神经病理性疼痛
伤害感受器
伤害
痛觉超敏
加巴喷丁
神经科学
医学
神经损伤
有害刺激
敏化
痛觉过敏
基础(医学)
麻醉
内科学
心理学
病理
受体
胰岛素
替代医学
作者
Changgeng Peng,Lili Li,Mingdong Zhang,Carolina Bengtsson Gonzales,Marc Parisien,Inna Belfer,Dmitry Usoskin,Hind Abdo,Alessandro Furlan,Martin Häring,François Lallemend,Tibor Harkany,Luda Diatchenko,Tomas Hökfelt,Jens Hjerling-Leffler,Patrik Ernfors
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2017-06-16
卷期号:356 (6343): 1168-1171
被引量:104
标识
DOI:10.1126/science.aam7671
摘要
Nociception is protective and prevents tissue damage but can also facilitate chronic pain. Whether a general principle governs these two types of pain is unknown. Here, we show that both basal mechanical and neuropathic pain are controlled by the microRNA-183 (miR-183) cluster in mice. This single cluster controls more than 80% of neuropathic pain-regulated genes and scales basal mechanical sensitivity and mechanical allodynia by regulating auxiliary voltage-gated calcium channel subunits α2δ-1 and α2δ-2. Basal sensitivity is controlled in nociceptors, and allodynia involves TrkB+ light-touch mechanoreceptors. These light-touch-sensitive neurons, which normally do not elicit pain, produce pain during neuropathy that is reversed by gabapentin. Thus, a single microRNA cluster continuously scales acute noxious mechanical sensitivity in nociceptive neurons and suppresses neuropathic pain transduction in a specific, light-touch-sensitive neuronal type recruited during mechanical allodynia.
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