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      Spinal Inhibitory Ptf1a-Derived Neurons Prevent Self-Generated Itch.

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          Abstract

          Chronic itch represents an incapacitating burden on patients suffering from a spectrum of diseases. Despite recent advances in our understanding of the cells and circuits implicated in the processing of itch information, chronic itch often presents itself without an apparent cause. Here, we identify a spinal subpopulation of inhibitory neurons defined by the expression of Ptf1a, involved in gating mechanosensory information self-generated during movement. These neurons receive tactile and motor input and establish presynaptic inhibitory contacts on mechanosensory afferents. Loss of Ptf1a neurons leads to increased hairy skin sensitivity and chronic itch, partially mediated by the classic itch pathway involving gastrin-releasing peptide receptor (GRPR) spinal neurons. Conversely, chemogenetic activation of GRPR neurons elicits itch, which is suppressed by concomitant activation of Ptf1a neurons. These findings shed light on the circuit mechanisms implicated in chronic itch and open novel targets for therapy developments.

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          Author and article information

          Journal
          Cell Rep
          Cell reports
          Elsevier BV
          2211-1247
          November 24 2020
          : 33
          : 8
          Affiliations
          [1 ] Department Molecules-Signaling-Development, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany. Electronic address: aescalante@neuro.mpg.de.
          [2 ] Department Molecules-Signaling-Development, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany. Electronic address: rklein@neuro.mpg.de.
          Article
          S2211-1247(20)31411-X
          10.1016/j.celrep.2020.108422
          33238109
          0d8ddaf3-22e2-4f4f-b018-10ac70b2844c
          Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.

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