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The Journal of Neuroscience, August 15, 2001, 21(16):6214-6220

Acute Neuronal Apoptosis in a Rat Model of Multiple Sclerosis

Roman Meyer2, Robert Weissert2, Ricarda Diem1, Maria K. Storch3, Katrien L. de Graaf2, Birgit Kramer1, and Mathias Bähr1

1 Neurologische Universitätsklinik, 37075 Göttingen, Germany, 2 Neurologische Universitätsklinik, 72076 Tübingen, Germany, and 3 Neurologische Universitätsklinik, 8036 Graz, Austria

Demyelination caused by inflammation of the CNS has been considered to be a major hallmark of multiple sclerosis (MS). Using experimental autoimmune encephalomyelitis, a model of MS, we demonstrate that an immune-mediated attack of the optic nerve is accompanied by an early degeneration of retinal ganglion cells (RGCs). The decrease of neuronal cell density was correlated with functional disabilities as assessed by visual evoked cortical potentials and electroretinogram. Visual acuity was significantly reduced. DNA degradation and activation of caspase-3 in RGCs indicate that cell death of RGCs is apoptotic. These findings show for the first time that an inflammatory attack against myelin components can lead to acute neuronal cell loss by apoptosis.

Key words: experimental autoimmune encephalomyelitis; visual evoked potentials; electroretinogram; CNS pathology; caspase-3; retinal ganglion cells

Copyright © 2001 Society for Neuroscience  0270-6474/01/21166214-07$05.00/0




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