Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute Disease
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Animals
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Apoptosis*
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Caspase 3
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Caspases / metabolism
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Cell Count
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DNA Fragmentation
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Demyelinating Diseases / pathology
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Disease Models, Animal*
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Electroretinography
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Encephalomyelitis, Autoimmune, Experimental / chemically induced
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Encephalomyelitis, Autoimmune, Experimental / pathology*
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Encephalomyelitis, Autoimmune, Experimental / physiopathology
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Evoked Potentials, Visual
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Female
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Freund's Adjuvant
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Inflammation / pathology
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Myelin Proteins
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Myelin-Associated Glycoprotein
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Myelin-Oligodendrocyte Glycoprotein
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Neurons / pathology*
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Optic Nerve / pathology
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Photic Stimulation
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Rats
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Rats, Inbred BN
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Retinal Ganglion Cells / pathology
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Visual Acuity
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Visual Cortex / physiopathology
Substances
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Mog protein, rat
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Myelin Proteins
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Myelin-Associated Glycoprotein
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Myelin-Oligodendrocyte Glycoprotein
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Freund's Adjuvant
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Casp3 protein, rat
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Caspase 3
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Caspases