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

• Verfasst von: Gritsch, Simon [VerfasserIn]
• Verfasst von: Lu, Jianning [VerfasserIn]
• Verfasst von: Kuner, Rohini [VerfasserIn]
• Titel: Oligodendrocyte ablation triggers central pain independently of innate or adaptive immune responses in mice
• Verf.angabe: 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 & Rohini Kuner
• E-Jahr: 2014
• Jahr: 01 December 2014
• Umfang: 17 S.
• Fussnoten: Gesehen am 20.10.2020
• Titel Quelle: Enthalten in: Nature Communications
• Ort Quelle: [London] : Nature Publishing Group UK, 2010
• Jahr Quelle: 2014
• Band/Heft Quelle: 5(2014) Artikel-Nummer 5472, 17 Seiten
• ISSN Quelle: 2041-1723
• DOI: doi:10.1038/ncomms6472
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1736014218

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.