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Dendritic and synaptic pathology in experimental autoimmune encephalomyelitis
Bing Zhu1, Liqing Luo, G R Wayne Moore
1Brain Research Center, Vancouver Hospitals and Health Sciences Center, The University of British Columbia, Vancouver, Canada. bzhu@rics.bwh.harvard.edu
The American Journal of Pathology
|April 23, 2003
Summary
Excitotoxicity damages spinal cord dendrites and synapses in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. This damage correlates with inflammation and may cause neurological deficits.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Excitotoxicity is implicated in central nervous system damage in multiple sclerosis and EAE.
- Dendrites and synapses are particularly vulnerable to excitotoxicity.
Purpose of the Study:
- To investigate dendritic and synaptic alterations in acute and chronic models of EAE.
- To correlate these structural changes with inflammatory processes and neurological deficits.
Main Methods:
- Utilized experimental autoimmune encephalomyelitis (EAE) models.
- Employed immunostaining for microtubule-associated protein-2 (MAP-2) to assess dendritic beading.
- Used retrograde labeling to identify beaded motoneuron dendrites.
- Quantified synaptic protein immunoreactivities (synaptophysin, synapsin I, PSD-95).
- Correlated pathological findings with inflammatory cell infiltration.
Main Results:
- Extensive dendritic beading observed in the white matter of the lumbosacral spinal cord (LSSC) during acute EAE and relapses.
- Dendritic beading showed significant recovery during EAE remission and recovery.
- Reduced immunoreactivity for synaptic proteins (synaptophysin, synapsin I, PSD-95) in both gray and white matter of the LSSC during acute EAE and relapses.
- Synaptic protein levels partially recovered during remission and recovery.
- Dendritic and synaptic damage correlated with inflammatory cell infiltration.
Conclusions:
- Dendritic and synaptic damage occurs in the spinal cord during EAE.
- These structural alterations are linked to inflammatory processes.
- Spinal cord dendritic and synaptic damage may contribute to neurological deficits observed in EAE.