首页> 美国卫生研究院文献>Molecular Pain >Imiquimod enhances excitability of dorsal root ganglion neurons by inhibiting background (K2P) and voltage-gated (Kv1.1 and Kv1.2) potassium channels
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Imiquimod enhances excitability of dorsal root ganglion neurons by inhibiting background (K2P) and voltage-gated (Kv1.1 and Kv1.2) potassium channels

机译:咪喹莫特通过抑制背景(K2P)和电压门控(Kv1.1和Kv1.2)钾通道来增强背根神经节神经元的兴奋性

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摘要

BackgroundImiquimod (IQ) is known as an agonist of Toll-like receptor 7 (TLR7) and is widely used to treat various infectious skin diseases. However, it causes severe itching sensation as its side effect. The precise mechanism of how IQ causes itching sensation is unknown. A recent report suggested a molecular target of IQ as TLR7 expressed in dorsal root ganglion (DRG) neurons. However, we recently proposed a TLR7-independent mechanism, in which the activation of TLR7 is not required for the action of IQ in DRG neurons. To resolve this controversy regarding the involvement of TLR7 and to address the exact molecular identity of itching sensation by IQ, we investigated the possible molecular target of IQ in DRG neurons.
机译:背景咪喹莫特(IQ)被称为Toll样受体7(TLR7)的激动剂,被广泛用于治疗各种传染性皮肤病。但是,它会引起严重的瘙痒感。智商如何引起瘙痒感觉的确切机制尚不清楚。最近的报告表明,智商的分子靶标是在背根神经节(DRG)神经元中表达的TLR7。但是,我们最近提出了一种独立于TLR7的机制,其中DRG神经元中IQ的作用不需要激活TLR7。为了解决有关TLR7参与的争议并解决IQ引起的瘙痒感觉的确切分子身份,我们研究了DRG神经元中IQ的可能分子靶标。

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