Acetylcholine receptor organization at the dystrophic extraocular muscle neuromuscular junction

dc.creatorMarques, MJ
dc.creatorPertille, A
dc.creatorCarvalho, CLT
dc.creatorSanto Neto, H
dc.date2007
dc.dateJUL
dc.date2014-11-16T04:07:01Z
dc.date2015-11-26T17:23:08Z
dc.date2014-11-16T04:07:01Z
dc.date2015-11-26T17:23:08Z
dc.date.accessioned2018-03-29T00:10:29Z
dc.date.available2018-03-29T00:10:29Z
dc.identifierAnatomical Record-advances In Integrative Anatomy And Evolutionary Biology. Wiley-liss, v. 290, n. 7, n. 846, n. 854, 2007.
dc.identifier1932-8486
dc.identifierWOS:000247821500011
dc.identifier10.1002/ar.20525
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/54095
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/54095
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/54095
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1283758
dc.descriptionSpared extraocular muscles of dystrophic mice are not subjected to regeneration process and can be used to verify whether the lack of dystrophin per se could cause changes in acetylcholine receptor (AChR) distribution. In the present study, rectus and oblique (spared) and retractor bulbi (nonspared) muscles were dissected from adult control (C57Bl/10) and mdx mice. AChRs and nerve terminals were labeled with rhodamine-a-bungarotoxin and anti-NF200-IgG-FITC, respectively, and visualized by confocal microscopy. Rectus and oblique muscles presented 0.5% central nucleation, while retractor bulbi had central nucleation in 45% of muscle fibers. In mdx rectus, AChRs were distributed in branches in 99% of the junctions examined (n = 200), similar to that observed for controls. Nerve terminals covered the AChR branches in 100% of the junctions examined. In control retractor bulbi, AChRs were distributed in regular branches. In mdx retractor bulbi, multiple fragmented islands of receptors were seen in 56% of the endplates examined (n = 200). These results suggest that the lack of dystrophin per se does not influence the distribution of acetylcholine receptors at the neuromuscular junction of spared extraocular muscles.
dc.description290
dc.description7
dc.description846
dc.description854
dc.languageen
dc.publisherWiley-liss
dc.publisherHoboken
dc.publisherEUA
dc.relationAnatomical Record-advances In Integrative Anatomy And Evolutionary Biology
dc.relationAnat. Rec.
dc.rightsfechado
dc.rightshttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.sourceWeb of Science
dc.subjectacetylcholine receptors
dc.subjectextraocular muscles
dc.subjectmdx mice
dc.subjectmuscle regeneration
dc.subjectneuromuscular junction
dc.subjectDuchenne Muscular-dystrophy
dc.subjectNitric-oxide Synthase
dc.subjectMdx Mice
dc.subjectEnd-plates
dc.subjectFibers
dc.subjectCell
dc.subjectExpression
dc.subjectMicroscopy
dc.subjectComplex
dc.subjectMouse
dc.titleAcetylcholine receptor organization at the dystrophic extraocular muscle neuromuscular junction
dc.typeArtículos de revistas


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