Mechanical hypersensitivity is a debilitating symptom associated with millions of chronic pain patients. It exists in distinct forms, including brush-evoked dynamic and filament-evoked punctate. Here we report that dynamic mechanical hypersensitivity induced by nerve injury or inflammation was compromised in mice with ablation of spinal VT3 Lbx1 neurons defined by coexpression of VGLUT3 Cre and Lbx1 Flpo , as indicated by the loss of brush-evoked nocifensive responses and conditional place aversion. Electrophysiological recordings show that VT3 Lbx1 neurons form morphine-resistant polysynaptic pathways relaying inputs from low-threshold Aβ mechanoreceptors to lamina I output neurons. Meanwhile, the subset of somatostatin (SOM) lineage neurons preserved in VT3 Lbx1 neuron-ablated mice is largely sufficient to mediate von Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms # Correspondence should be addressed to yunwang@fudan.edu.cn or Qiufu_Ma@dfci.harvard.edu. * These authors contributed equally to this study. Competing Financial InterestsThe authors declare no competing financial interests. HHS Public AccessAuthor manuscript Nat Neurosci. Author manuscript; available in PMC 2017 October 24. Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptFrey filament-evoked punctate mechanical hypersensitivity, including both morphine-sensitive and morphine-resistant forms. Furthermore, acute silencing of VT3 Lbx1 neurons attenuated preestablished dynamic mechanical hypersensitivity induced by nerve injury, suggesting these neurons as a potential cellular target for treating this form of neuropathic pain.

Gate-tunable inverse Edelstein effect is observed at room temperature in Rashba-split 2DEG at the complex oxide interface.

We report direct experimental signatures for the spin superfluid ground state in canted antiferromagnets via nonlocal spin transport.