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首页> 外文期刊>Molecular brain >Extracellular signal-regulated kinase (ERK) activation is required for itch sensation in the spinal cord
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Extracellular signal-regulated kinase (ERK) activation is required for itch sensation in the spinal cord

机译：脊髓瘙痒感需要细胞外信号调节激酶（ERK）激活

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Background Itch, chronic itch in particular, can have a significant negative impact on an individual’s quality of life. However, the molecular mechanisms underlying itch processing in the central nervous system remain largely unknown. Results We report here that activation of ERK signaling in the spinal cord is required for itch sensation. ERK activation, as revealed by anti-phosphorylated ERK1/2 immunostaining, is observed in the spinal dorsal horn of mice treated with intradermal injections of histamine and compound 48/80 but not chloroquine or SLIGRL-NH2, indicating that ERK activation only occurs in histamine-dependent acute itch. In addition, ERK activation is also observed in 2, 4-dinitrofluorobenzene (DNFB)-induced itch. Consistently, intrathecal administration of the ERK phosphorylation inhibitor U0126 dramatically reduces the scratching behaviors induced by histamine and DNFB, but not by chloroquine. Furthermore, administration of the histamine receptor H1 antagonist chlorpheniramine decreases the scratching behaviors and ERK activation induced by histamine, but has no effect on DNFB-induced itch responses. Finally, the patch-clamp recording shows that in histamine-, chloroquine- and DNFB-treated mice the spontaneous excitatory postsynaptic current (sEPSC) of dorsal horn neurons is increased, and the decrease of action potential threshold is largely prevented by bathing of U0126 in histamine- and DNFB-treated mice but not those treated with chloroquine. Conclusion Our results demonstrate a critical role for ERK activation in itch sensation at the spinal level.
机译：背景瘙痒（尤其是慢性瘙痒）可能会对个人的生活质量产生重大的负面影响。然而，在中枢神经系统中瘙痒处理的分子机制仍是未知之数。结果我们在此报告，痒感需要激活脊髓中的ERK信号。如通过抗磷酸化ERK1 / 2免疫染色所揭示的，在皮内注射组胺和化合物48/80而不是氯喹或SLIGRL-NH2处理的小鼠的脊髓背角中观察到ERK活化，表明ERK活化仅在组胺中发生依赖性急性瘙痒。此外，在2，4-二硝基氟苯（DNFB）引起的瘙痒中也观察到ERK活化。一致地，鞘内施用ERK磷酸化抑制剂U0126显着降低了由组胺和DNFB诱导的the抓行为，但没有减少由氯喹引起的抓挠行为。此外，组胺受体H1拮抗剂扑尔敏的给药减少了由组胺引起的抓挠行为和ERK活化，但对DNFB引起的瘙痒反应没有影响。最后，膜片钳记录表明，在组胺，氯喹和DNFB处理的小鼠中，背角神经元的自发性兴奋性突触后突触电流（sEPSC）增加，而在U0126上洗澡可很大程度上防止动作电位阈值的降低。组胺和DNFB处理的小鼠，但未用氯喹处理的小鼠。结论我们的结果表明ERK激活在脊柱水平的瘙痒感中起着关键作用。

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