Oligodendrocyte ablation triggers central pain independently of innate or adaptive immune responses in mice

Simon Gritsch, Jianning Lu, Sebastian Thilemann, Simone Wörtge, Wiebke Möbius, Julia Bruttger, Khalad Karram, Torben Ruhwedel, Michaela Blanfeld, Daniel Vardeh, Ari Waisman, Klaus-Armin Nave and Rohini Kuner ()
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Simon Gritsch: Institute for Pharmacology, University of Heidelberg
Jianning Lu: Institute for Pharmacology, University of Heidelberg
Sebastian Thilemann: Institute for Pharmacology, University of Heidelberg
Simone Wörtge: Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz
Wiebke Möbius: Max Planck Institute of Experimental Medicine
Julia Bruttger: Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz
Khalad Karram: Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz
Torben Ruhwedel: Max Planck Institute of Experimental Medicine
Michaela Blanfeld: Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz
Daniel Vardeh: Institute for Pharmacology, University of Heidelberg
Ari Waisman: Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz
Klaus-Armin Nave: Max Planck Institute of Experimental Medicine
Rohini Kuner: Institute for Pharmacology, University of Heidelberg

Nature Communications, 2014, vol. 5, issue 1, 1-17

Abstract: Abstract Mechanisms underlying central neuropathic pain are poorly understood. Although glial dysfunction has been functionally linked with neuropathic pain, very little is known about modulation of pain by oligodendrocytes. Here we report that genetic ablation of oligodendrocytes rapidly triggers a pattern of sensory changes that closely resemble central neuropathic pain, which are manifest before overt demyelination. Primary oligodendrocyte loss is not associated with autoreactive T- and B-cell infiltration in the spinal cord and neither activation of microglia nor reactive astrogliosis contribute functionally to central pain evoked by ablation of oligodendrocytes. Instead, light and electron microscopic analyses reveal axonal pathology in the spinal dorsal horn and spinothalamic tract concurrent with the induction and maintenance of nociceptive hypersensitivity. These data reveal a role for oligodendrocytes in modulating pain and suggest that perturbation of oligodendrocyte functions that maintain axonal integrity can lead to central neuropathic pain independent of immune contributions.

Date: 2014
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DOI: 10.1038/ncomms6472

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