期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-09405-9
关键词
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资金
- Multiple Sclerosis Research Australia
- Trish Multiple Sclerosis Research Foundation Postgraduate Scholarship
- National Multiple Sclerosis Society Project [RG4398A1/1]
- International Progressive Multiple Sclerosis Alliance Challenge Award [PA0065]
- Trish Multiple Sclerosis Research Foundation [15-022]
- Bethlehem Griffiths Research Foundation [BGRF1706]
Axo-glial units are highly organised microstructures propagating saltatory conduction and are disrupted during multiple sclerosis (MS). Nogo receptor 1 (NgR1) has been suggested to govern axonal damage during the progression of disease in the MS-like mouse model, experimental autoimmune encephalomyelitis (EAE). Here we have identified that adult ngr1(-/-) mice, previously used in EAE and spinal cord injury experime(n)ts, display elongated paranodes, and nodes of Ranvier. Unstructured paranodal regions in ngr1(-/-) mice are matched with more distributed expression pattern of Caspr. Compound action potentials of optic nerves and spinal cords from naive ngr1(-/-) mice are delayed and reduced. Molecular interaction studies revealed enhanced Caspr cleavage. Our data suggest that NgR1 may regulate axo-myelin ultrastructure through Caspr-mediated adhesion, regulating the electrophysiological signature of myelinated axons of central nervous system (CNS).
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