Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the 
central nervous system (CNS). Recent studies suggest that, beside focal lesions, 
diffuse inflammatory and degenerative processes take place throughout the MS 
brain. Especially, molecular alterations in the so-called normal appearing white 
matter suggest the induction of neuroprotective mechanisms against oxidative 
stress preserving cellular homeostasis and function. In this study we 
investigated whether in an animal model for MS, namely in experimental 
autoimmune encephalomyelitis (EAE), similar changes occur. We isolated normal 
appearing white and grey matter from the corpus callosum and the above lying 
cerebral cortex from DA rats with rMOG-induced EAE and carried out a gene 
expression analysis. Examination of corpus callosum revealed only minor changes 
in EAE rats. In contrast, we identified a number of gene expression alterations 
in the cerebral cortex even though morphological and cellular alterations were 
not evident. One of the most striking observations was the downregulation of 
genes involved in mitochondrial function as well as a whole set of genes coding 
for different glutamate receptors. Our data imply that molecular alterations are 
present in neurons far distant to inflammatory demyelinating lesions. These 
alterations might reflect degenerative processes induced by lesion-mediated 
axonal injury in the spinal cord. Our results indicate that the MOG-induced EAE 
in DA rats is a valuable model to analyze neuronal alterations due to axonal 
impairment in an acute phase of a MS-like disease, and could be used for 
development of neuroprotective strategies.