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Whole-mount Imaging of Mouse Embryo Sensory Axon Projections
Published on: December 9, 2014
Enhanced visualization of axonopathy in EAE using thy1-YFP transgenic mice
1Neurology Research, Shriners Hospital for Children, Sacramento, CA 95817, United States. pgbannerman@ucdavis.edu
Journal of the Neurological Sciences
|May 12, 2007
Summary
This study reveals axonal damage in a mouse model of multiple sclerosis (MS). Combining YFP fluorescence and neurofilament markers offers a detailed view of axonopathy and early inflammatory attacks on axons in the spinal cord.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Chronic disabilities in multiple sclerosis (MS) are linked to neuronal damage.
- Understanding axonal disruption is crucial for developing MS therapies.
Purpose of the Study:
- To characterize axonal damage in the spinal cord of mice with MOG-induced experimental autoimmune encephalomyelitis (MOG-EAE), an MS model.
- To investigate the utility of YFP reporter mice and specific antibodies for visualizing axonal pathology.
Main Methods:
- Induced MOG-EAE in thy1-YFP transgenic mice.
- Utilized YFP fluorescence to track motorneurons and SMI 32 antibody for hypophosphorylated neurofilament-H (hypoP-NF-H).
- Employed CD11b antibody to identify inflammatory cells and assess their interaction with axons.
Main Results:
- Observed fragmented axons and axonal spheroids in MOG-EAE mice.
- Found that YFP and hypoP-NF-H markers visualized distinct populations of damaged axons, providing a more comprehensive assessment.
- Detected early inflammatory cell attack on white matter axons using YFP and CD11b.
- Showed accumulation of hyperphosphorylated neurofilament-H (hyperP-NF-H) in lesioned areas and neuronal perikarya.
Conclusions:
- Combining YFP fluorescence and hypoP-NF-H immunoreactivity offers a more complete picture of axonopathy in the MOG-EAE spinal cord.
- This approach aids in identifying early inflammatory processes targeting axons in MS models.
- The findings contribute to understanding neurodegeneration mechanisms in MS.

