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A newly discovered cell type for pain perception

Pain has been thought to be initiated by activation of free nerve endings without end organs in the skin. In contrast to this paradigm, Abdo et al. discovered a previously unknown meshlike organ covering the skin that senses dangerous environmental stimuli (see the Perspective by Doan and Monk). This organ is built from specialized glial cells located in the epidermal-dermal border and is sufficient and required for initiation of mechanical pain transduction.
Science, this issue p. 695; see also p. 641

Abstract

An essential prerequisite for the survival of an organism is the ability to detect and respond to aversive stimuli. Current belief is that noxious stimuli directly activate nociceptive sensory nerve endings in the skin. We discovered a specialized cutaneous glial cell type with extensive processes forming a mesh-like network in the subepidermal border of the skin that conveys noxious thermal and mechanical sensitivity. We demonstrate a direct excitatory functional connection to sensory neurons and provide evidence of a previously unknown organ that has an essential physiological role in sensing noxious stimuli. Thus, these glial cells, which are intimately associated with unmyelinated nociceptive nerves, are inherently mechanosensitive and transmit nociceptive information to the nerve.
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Science
Volume 365Issue 645416 August 2019
Pages: 695 - 699

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Received: 10 April 2019
Accepted: 2 July 2019

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Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Neuroscience, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm 17177, Sweden.
Abdeljabbar El Manira
Department of Neuroscience, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm 17177, Sweden.
Department of Medical Biochemistry and Biophysics, Division of Molecular Neurobiology, Karolinska Institutet, Stockholm 17177, Sweden.

Notes

*
These authors contributed equally to this work.
†Corresponding author. Email: [email protected]

Funding Information

http://dx.doi.org/10.13039/100004440Wellcome Trust:
http://dx.doi.org/10.13039/501100000781European Research Council: PainCells 740491
http://dx.doi.org/10.13039/501100004047Karolinska Institutet:
http://dx.doi.org/10.13039/501100004063Knut och Alice Wallenbergs Stiftelse:
http://dx.doi.org/10.13039/501100004359Vetenskapsrådet:

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Science
Volume 365|Issue 6454
16 August 2019
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Received:10 April 2019
Accepted:2 July 2019
Published in print:16 August 2019
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