<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7(1)</volume><submitter>Lee JY</submitter><pubmed_abstract>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 &lt;sup>-/-&lt;/sup> mice, previously used in EAE and spinal cord injury experiments, display elongated paranodes, and nodes of Ranvier. Unstructured paranodal regions in ngr1 &lt;sup>-/-&lt;/sup> mice are matched with more distributed expression pattern of Caspr. Compound action potentials of optic nerves and spinal cords from naïve ngr1 &lt;sup>-/-&lt;/sup> 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).</pubmed_abstract><journal>Scientific reports</journal><pagination>8958</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5567129</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Nogo receptor 1 regulates Caspr distribution at axo-glial units in the central nervous system.</pubmed_title><pmcid>PMC5567129</pmcid><pubmed_authors>Aui PM</pubmed_authors><pubmed_authors>Petratos S</pubmed_authors><pubmed_authors>Fehlings MG</pubmed_authors><pubmed_authors>Kim MJ</pubmed_authors><pubmed_authors>Velumian AA</pubmed_authors><pubmed_authors>Lee JY</pubmed_authors><pubmed_authors>Li L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Nogo receptor 1 regulates Caspr distribution at axo-glial units in the central nervous system.</name><description>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 &lt;sup>-/-&lt;/sup> mice, previously used in EAE and spinal cord injury experiments, display elongated paranodes, and nodes of Ranvier. Unstructured paranodal regions in ngr1 &lt;sup>-/-&lt;/sup> mice are matched with more distributed expression pattern of Caspr. Compound action potentials of optic nerves and spinal cords from naïve ngr1 &lt;sup>-/-&lt;/sup> 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).</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Aug</publication><modification>2024-11-13T02:04:29.523Z</modification><creation>2019-03-27T02:54:11Z</creation></dates><accession>S-EPMC5567129</accession><cross_references><pubmed>28827698</pubmed><doi>10.1038/s41598-017-09405-9</doi></cross_references></HashMap>