| First Author | Lee JY | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 8958 |
| PubMed ID | 28827698 | Mgi Jnum | J:256573 |
| Mgi Id | MGI:6108677 | Doi | 10.1038/s41598-017-09405-9 |
| Citation | Lee JY, et al. (2017) Nogo receptor 1 regulates Caspr distribution at axo-glial units in the central nervous system. Sci Rep 7(1):8958 |
| abstractText | 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 experiments, 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). |
