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TRPV1 activity and substance P release are required for corneal cold nociception

Author

Listed:
  • Fengxian Li

    (Washington University School of Medicine
    Zhujiang Hospital of Southern Medical University)

  • Weishan Yang

    (Washington University School of Medicine)

  • Haowu Jiang

    (Washington University School of Medicine)

  • Changxiong Guo

    (Washington University School of Medicine)

  • Andrew J. W. Huang

    (Washington University School of Medicine)

  • Hongzhen Hu

    (Washington University School of Medicine)

  • Qin Liu

    (Washington University School of Medicine
    Washington University School of Medicine)

Abstract

As a protective mechanism, the cornea is sensitive to noxious stimuli. Here, we show that in mice, a high proportion of corneal TRPM8+ cold-sensing fibers express the heat-sensitive TRPV1 channel. Despite its insensitivity to cold, TRPV1 enhances membrane potential changes and electrical firing of TRPM8+ neurons in response to cold stimulation. This elevated neuronal excitability leads to augmented ocular cold nociception in mice. In a model of dry eye disease, the expression of TRPV1 in TRPM8+ cold-sensing fibers is increased, and results in severe cold allodynia. Overexpression of TRPV1 in TRPM8+ sensory neurons leads to cold allodynia in both corneal and non-corneal tissues without affecting their thermal sensitivity. TRPV1-dependent neuronal sensitization facilitates the release of the neuropeptide substance P from TRPM8+ cold-sensing neurons to signal nociception in response to cold. Our study identifies a mechanism underlying corneal cold nociception and suggests a potential target for the treatment of ocular pain.

Suggested Citation

  • Fengxian Li & Weishan Yang & Haowu Jiang & Changxiong Guo & Andrew J. W. Huang & Hongzhen Hu & Qin Liu, 2019. "TRPV1 activity and substance P release are required for corneal cold nociception," Nature Communications, Nature, vol. 10(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13536-0
    DOI: 10.1038/s41467-019-13536-0
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