Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/22705
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dc.contributor.authorCai, Z.en
dc.contributor.authorFinnie, J.en
dc.contributor.authorBlumbergs, P.en
dc.contributor.authorManavis, J.en
dc.contributor.authorGhabriel, M.en
dc.contributor.authorThompson, P.en
dc.date.issued2006en
dc.identifier.citationExperimental Neurology, 2006; 198(1):65-71en
dc.identifier.issn0014-4886en
dc.identifier.issn1090-2430en
dc.identifier.urihttp://hdl.handle.net/2440/22705-
dc.descriptionCopyright © 2005 Elsevier Inc. All rights reserved.en
dc.description.abstractIntroduction Disruption of the complex architectural and molecular organization of the paranodal region of myelinated peripheral nerve fiber may initiate the evolving time dependent process of segmental demyelination. In support of this notion was the finding of focal paranodal myelin swellings (tomacula) due to redundant folding of myelin sheaths, early in the time course of an avian riboflavin deficiency model of demyelinating neuropathy. Methods Newborn broiler meat chickens were maintained either on a routine diet containing 5.0 mg/kg riboflavin (control group) or a riboflavin-deficient diet containing 1.8 mg/kg riboflavin. Riboflavin concentrations in the liver were measured at postnatal day 11. Peripheral nerves were morphologically examined at days 6, 11, 16 and 21 using light and electron microscopy and teased nerve fiber techniques. Results Riboflavin-deficient chickens showed signs of a neuropathy from days 8 and pathological examination of peripheral nerves revealed a demyelinating neuropathy with paranodal tomacula formation starting on day 11. Paranodal tomacula consisted of redundant myelin infoldings or outfoldings, increased in size and frequency after day 11. After day 16, the paranodal swellings showed prominent degenerative changes accompanied by an increased frequency of myelinated fibers showing demyelination. Conclusion Tomacula due to redundant myelin folds are generally considered a remyelination phenomenon, yet in this avian riboflavin deficiency model of demyelination, the paranodal tomacula occurred early in the course of demyelination.en
dc.description.statementofresponsibilityZ. Cai, J.W. Finnie, P.C. Blumbergs, J. Manavis, Mounir N. Ghabriel and P.D. Thompsonen
dc.language.isoenen
dc.publisherAcademic Press Inc Elsevier Scienceen
dc.subjectriboflavin; demyelinating neuropathy; tomacula; paranodeen
dc.titleEarly paranodal myelin swellings (tomacula) in an avian riboflavin deficiency model of demyelinating neuropathyen
dc.typeJournal articleen
dc.identifier.rmid0020060102en
dc.identifier.doi10.1016/j.expneurol.2005.10.028en
dc.identifier.pubid53235-
pubs.library.collectionAnatomical Sciences publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidGhabriel, M. [0000-0002-9153-271X]en
Appears in Collections:Anatomical Sciences publications

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