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57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

12. - 15.09.2012, Erlangen

Banner: 57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie

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Rescue of oligodendroglia in experimental NMO lesions

Meeting Abstract

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  • presenting/speaker Claudia Wrzos - Uniklinikum Göttingen, Neuropathologie, Göttingen, Germany
  • Jeffrey Bennett - Uniklinikum Göttingen, Neuropathologie, Göttingen, United States
  • Wolfgang Brück - Uniklinikum Göttingen, Neuropathologie, Göttingen, Germany
  • Stefan Nessler - Uniklinikum Göttingen, Neuropathologie, Göttingen, Germany
  • Christine Stadelmann - Uniklinikum Göttingen, Neuropathologie, Göttingen, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP2.5

doi: 10.3205/12dgnn041, urn:nbn:de:0183-12dgnn0411

Veröffentlicht: 11. September 2012

© 2012 Wrzos et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.

Gliederung

Text

Neuromyelitis optica (NMO) is an inflammatory-demyelinating disease characterized by destructive lesions in the optic nerves and spinal cord. In addition to astrocyte depletion, oligodendroglial cells are lost in NMO lesions. However, the time course and mechanisms of oligodendroglial demise have not been characterized in detail.

In our study we used monoclonal antibodies against Aquaporin 4 (AQP4) reconstructed from CSF plasma cells of NMO patients. These rAbs have recently been shown to deplete perivascular astrocytes if i.v. injected into MBP- primed rats (Bennett et al., 2009).

Already 24 hrs after a single stereotactic intracerebral injection of a complement-binding anti-AQP4 antibody diluted in human serum into the rat brain, the peak of astrocyte depletion was achieved. Similarly, loss of oligodendroglia occurred rapidly and was nearly complete at this time point. In vitro, oligodendroglial cells were damaged after incubation with supernatant from astrocytes previously incubated with anti-AQP4 antibody and human complement. Oligodendroglial cell death was partly blocked by NMDA and other receptor antagonists in vitro and in vivo.

Our results suggest a role for excitotixicity in oligodendroglial reduction in experimental NMO lesions.