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Nfia-dependent mechanoreceptors are required for dynamic mechanical hypersensitivity after nerve injury

Nfia-dependent mechanoreceptors are required for dynamic mec...

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中国神经科学学会第十二届全国学术会议

作者： Lu QI Qiuyi GU Xiaohua WU Guangjuan YIN Lu HAN Mengsheng QIU Richard M.GRONOSTAJSKI Qiufu MA Yang LIU Zhejiang Key Laboratory of Organ Development and Regeneration Institute of Life Sciences Hangzhou Normal University College of Life Sciences Zhejiang University Department of Biochemistry Program in Genetics Genomics and BioinformaticsCenter of Excellence in Bioinformatics and Life Sciences State University of New York at Buffalo Dana-Farber Cancer Institute Harvard Medical School Department of Neurobiology Harvard Medical School

Mechanical allodynia represents an excruciating chronic pain resulted from lesions or inflammation to somatosensory system. Different forms of mechanical hypersensitivities, including brush-evoked dynamic and filament-evoked punctate(static) allodynia, recruit distinct circuits for signal transmission. A group of v Glut3-expressing excitatory spinal neurons is identified to preferentially transmit dynamic mechanical pain information after nerve injury and inflammation. However, what types of peripheral sensory and spinal inhibitory neurons specifically mediate dynamic allodynia in neuropathic or inflammatory conditions is still unknown. Here, we report that a group of Nuclear Factor I/A(Nfia)-dependent myelinated mechanoreceptors is particularly required for dynamic allodynia manifestation after nerve injury. Nfia conditional knockout(c KO) mice generated by using Nav1.8-Cre(Nfia;Nav1.8-Cre), in which only subsets of myelinated Aβ and Aδ neurons in the dorsal root ganglia(DRG) are affected, exhibit specific loss of dynamic, but not static allodynia in neuropathic pain model, while both forms of allodynia remain intact in CFA-induced inflammatory pain model. Reduced brush-evoked c-Fos signals in the dorsal spinal cord indicate the impairment of signal transduction in these mice. Furthermore, removal of GABA inhibition by intrathecal injection of Bicuculline induces severe mechanical hypersensitivities in wildtype mice, but fails in NfiaF/F;Nav1.8-Cre mice, implying that GABA spinal neurons constitute a "gate" controlling the transmission of mechanical allodynia information from these Nfia-dependent sensory neurons. In contrast, disinhibition of glycinergic spinal neurons by Strychnine evokes intact dynamic and static allodynia in the Nfia cKO mice, suggesting a more important role of glycinergic spinal neurons in gating inflammatory pain signals. These results distinguish different sensory and spinal neuronal components mediating dynamic allodynia in neuropathic and

关键词： dynamic allodynia Nuclear Factor I/A primary sensory neurons GABAA spinal inhibitory neurons

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