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57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

12. - 15.09.2012, Erlangen

57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

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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

Published: September 11, 2012

© 2012 Wrzos et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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.