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Nat Neurosci. 2017 Jun;20(6):804-814. doi: 10.1038/nn.4549. Epub 2017 Apr 24.

Identification of spinal circuits involved in touch-evoked dynamic mechanical pain.

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Institute of Brain Science, the State Key Laboratory of Medical Neurobiology and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Dana-Farber Cancer Institute and Department of Neurobiology, Harvard Medical School, Boston, Massachusetts, USA.
Cell Electrophysiology Laboratory, Wannan Medical College, Wuhu, China.
Molecular Neurobiology Laboratory, the Salk Institute for Biological Studies, La Jolla, California, USA.
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.


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 Aβ 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.

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