{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T05:33:12Z","timestamp":1790659992633,"version":"4.1.0"},"reference-count":55,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2017,4,3]],"date-time":"2017-04-03T00:00:00Z","timestamp":1491177600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["GM063074"],"award-info":[{"award-number":["GM063074"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["NS050356"],"award-info":[{"award-number":["NS050356"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000890","name":"National Multiple Sclerosis Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000890","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["(F32NS092448)"],"award-info":[{"award-number":["(F32NS092448)"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2017,7]]},"abstract":"<jats:p>\n                    Bidirectional interactions between neurons and myelinating glial cells result in formation of axonal domains along myelinated fibers. Loss of axonal domains leads to detrimental consequences on nerve structure and function, resulting in reduced conductive properties and the diminished ability to reliably transmit signals to the targets they innervate. Thus, impairment of peripheral myelinated axons that project to the surface of muscle fibers and form neuromuscular junction (NMJ) synapses leads to muscle dysfunction. The goal of our studies was to determine how altered electrophysiological properties due to axonal domain disorganization lead to muscle pathology, which is relevant to a variety of peripheral neuropathies, demyelinating diseases, and neurodegenerative disorders. Using conventional\n                    <jats:italic>Contactin<\/jats:italic>\n                    \u2010\n                    <jats:italic>Associated Protein 1<\/jats:italic>\n                    (\n                    <jats:italic>Caspr1<\/jats:italic>\n                    ) and\n                    <jats:italic>Caspr2<\/jats:italic>\n                    single or double mutants with disrupted paranodal, juxtaparanodal, or both regions, respectively, in peripheral myelinated axons, we correlated defects in NMJ integrity and muscle pathology. Our data show that loss of axonal domains in\n                    <jats:italic>Caspr1<\/jats:italic>\n                    and\n                    <jats:italic>Caspr2<\/jats:italic>\n                    single and double mutants primarily alters distal myelinated fibers together with presynaptic terminals, eventually leading to NMJ denervation and reduction in postsynaptic endplate areas. Moreover, reduction in conductive properties of peripheral myelinated fibers together with NMJ disintegration leads to muscle atrophy in\n                    <jats:italic>Caspr1<\/jats:italic>\n                    mutants or muscle fiber degeneration accompanied by mitochondrial dysfunction in\n                    <jats:italic>Caspr1<\/jats:italic>\n                    \/\n                    <jats:italic>Caspr2<\/jats:italic>\n                    double mutants. Together, our data indicate that proper organization of axonal domains in myelinated fibers is critical for optimal propagation of electrical signals, NMJ integrity, and muscle health, and provide insights into a wide range of pathologies that result in reduced nerve conduction leading to muscle atrophy. \u00a9 2017 Wiley Periodicals, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jnr.24052","type":"journal-article","created":{"date-parts":[[2017,4,5]],"date-time":"2017-04-05T09:21:21Z","timestamp":1491384081000},"page":"1373-1390","source":"Crossref","is-referenced-by-count":21,"title":["Axonal domain disorganization in\n                    <i>Caspr1<\/i>\n                    and\n                    <i>Caspr2<\/i>\n                    mutant myelinated axons affects neuromuscular junction integrity, leading to muscle atrophy"],"prefix":"10.1002","volume":"95","author":[{"given":"Julia","family":"Saifetiarova","sequence":"first","affiliation":[{"name":"Department of Cellular and Integrative Physiology, Center for Biomedical Neuroscience, School of Medicine University of Texas Health Science Center San Antonio Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xi","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, Center for Biomedical Neuroscience, School of Medicine University of Texas Health Science Center San Antonio Texas"},{"name":"Xiangya School of Medicine Central South University Changsha China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna M.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, Center for Biomedical Neuroscience, School of Medicine University of Texas Health Science Center San Antonio Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, Center for Biomedical Neuroscience, School of Medicine University of Texas Health Science Center San Antonio Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0989-1498","authenticated-orcid":false,"given":"Manzoor A.","family":"Bhat","sequence":"additional","affiliation":[{"name":"Department of Cellular and Integrative Physiology, Center for Biomedical Neuroscience, School of Medicine University of Texas Health Science Center San Antonio Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,4,3]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1216398109"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/jns5.12057"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.60.3.329"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.94.12.6054"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcn.2016.11.004"},{"key":"e_1_2_11_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(01)00294-X"},{"key":"e_1_2_11_8_1","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00028.2001"},{"key":"e_1_2_11_9_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1015-11.2011"},{"key":"e_1_2_11_10_1","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.23197"},{"key":"e_1_2_11_11_1","first-page":"659","article-title":"The \u201cdying back\u201d process. 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