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Brain Advance Access published online on May 18, 2005
Brain, doi:10.1093/brain/awh550
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received February 11, 2005
Revised April 4, 2005
Accepted April 21, 2005

Article

Motor neuron pathology in experimental autoimmune encephalomyelitis: studies in THY1-YFP transgenic mice

P. G. Bannerman 1, A. Hahn 1, S. Ramirez 1, M. Morley 1, C. Bönnemann 1, S. Yu 2, G.-X. Zhang 2, A. Rostami 2, and D. Pleasure 1*

1 Neurology Research, Abramson Pediatric Research Center, Children's Hospital of Philadelphia, Philadelphia, Pennsylvannia, USA
2 Department of Neurology, Thomas Jefferson Hospital, Philadelphia, Pennsylvannia, USA

* To whom correspondence should be addressed.
D. Pleasure, E-mail: pleasure{at}email.chop.edu


  Abstract

Using adult male C57BL/6 mice that express a yellow fluorescent protein transgene in their motor neurons, we induced experimental autoimmune encephalomyelitis (EAE) by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG peptide) in complete Freund's adjuvant (CFA). Control mice of the same transgenic strain received CFA without MOG peptide. Early in the course of their illness, the EAE mice showed lumbosacral spinal cord inflammation, demyelination and axonal fragmentation. By 14 weeks post-MOG peptide, these abnormalities were much less prominent, but the mice remained weak and, as in patients with progressive multiple sclerosis, spinal cord atrophy had developed. There was no significant loss of lumbar spinal cord motor neurons in the MOG peptide-EAE mice. However, early in the course of the illness, motor neuron dendrites were disrupted and motor neuron expression of hypophosphorylated neurofilament-H (hypoP-NF-H) immunoreactivity was diminished. By 14 weeks post-MOG peptide, hypoP-NF-H expression had returned to normal, but motor neuron dendritic abnormalities persisted and motor neuron perikaryal atrophy had appeared. We hypothesize that these motor neuron abnormalities contribute to weakness in this form of EAE and speculate that similar motor neuron abnormalities are present in patients with progressive multiple sclerosis.

Keywords: motor neuron; experimental autoimmune encephalomyelitis (EAE); dendrite; axonal degeneration; multiple sclerosis.
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