Axonal Transport Reductions in Acute Experimental Allergic Encephalomyelitis: Qualitative Analysis of the Optic Nerve
Autor: | E. Ann Ellis, Ernest F. Tark, Narsing A. Rao, John Guy, G. Marion Hope |
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Rok vydání: | 1989 |
Předmět: |
Retinal Ganglion Cells
Lamina Pathology medicine.medical_specialty Encephalomyelitis Autoimmune Experimental Silver Time Factors Macromolecular Substances Encephalomyelitis Guinea Pigs Neurotransmission Guinea pig Cellular and Molecular Neuroscience Leucine medicine Animals Demyelinating Disorder Cytoskeleton business.industry Biological Transport Optic Nerve medicine.disease Axons Sensory Systems Microscopy Electron Ophthalmology Optic nerve Axoplasmic transport Autoradiography business |
Zdroj: | Current Eye Research. 8:261-269 |
ISSN: | 1460-2202 0271-3683 |
DOI: | 10.3109/02713688908997568 |
Popis: | In order to determine if changes in axonal transport were different in adult animals with acute experimental allergic encephalomyelitis (EAE), in comparison to juvenile animals with chronic EAE, the effects of this acute demyelinating disorder on axonal transport were examined in the optic nerves of adult strain-13 guinea pigs. Utilizing autoradiographic analysis of silver grain counts, both the fast and slow components of orthograde transport were studied at intervals of thirty minutes, three hours, one day and three days after tritiated leucine injection into the vitreous cavity. In order to determine the contribution of fiber loss in acute EAE, optic nerve fiber density was analyzed from electron micrographs of normal and demyelinated nerves. Animals with acute EAE had a decrease in radioactivity at the lamina retinalis and lamina choroidalis after thirty minutes and three hours, and at the lamina scleralis and foci of demyelination after one and three days. A 16% loss of fibers did not account for as much as a 74% reduction in radioactivity with acute EAE. The global reductions in axonal transport observed in acute EAE animals may contribute to their progressive deterioration and eventual demise by lack of delivery of tubulo-vesicular materials for synaptic transmission, axolemmal proteins for electrogenesis and neurofilamentary components of the cytoskeleton. Moreover, they are unlike the increase of fast axonal transport associated with recovery of physiologic function characteristic of animals with the chronic form of the disease. |
Databáze: | OpenAIRE |
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