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Nature neurosci——VGLUT3+Lbx1+神经元介导了接触诱导的机械痛

已有 3977 次阅读 2017-5-1 12:03 |个人分类:神经科学临床和基础|系统分类:观点评述| style, color, center, important, 神经元

Nature neurosci——VGLUT3+Lbx1+神经元介导了接触诱导的机械痛

下面这一项是来自复旦大学脑科学研究院王云老师课题组的研究，成果是和哈佛大学合作发表的。他们发现了一类脊髓神经元VGLUT3+Lbx1+神经元为神经痛的感觉传入所必需。如果剔除这类神经元，小鼠就不能很好的对痛觉进行传导，而另一类SOM+神经元则传导的是吗啡敏感和Von frey纤维敏感的机械超敏信号。摘要如下：
Mechanical hypersensitivity is a debilitating symptom for millions of chronic pain patients. It exists in distinct forms, including brush-evoked dynamic and filament-evoked punctate hypersensitivities. We reduced dynamic mechanical hypersensitivity induced by nerve injury or inflammation in mice by ablating a group of adult spinal neurons defined by developmental co-expression of VGLUT3 and Lbx1 (VT3Lbx1 neurons): the mice lost brush-evoked nocifensive responses and conditional place aversion. Electrophysiological recordings show that VT3Lbx1 neurons form morphine-resistant polysynaptic pathways relaying inputs from low-threshold Ab mechanoreceptors to lamina I output neurons. The subset of somatostatin-lineage neurons preserved in VT3Lbx1-neuron-ablated mice is largely sufficient to mediate morphine-sensitive and morphine-resistant forms of von Frey filament-evoked punctate mechanical hypersensitivity. Furthermore, acute silencing of VT3Lbx1 neurons attenuated pre-established dynamic mechanical hypersensitivity induced by nerve injury, suggesting that these neurons may be a cellular target for treating this form of neuropathic pain.