dc.creatorOliveira, ALR
dc.creatorThams, S
dc.creatorLidman, O
dc.creatorPiehl, F
dc.creatorHokfelt, T
dc.creatorKarre, K
dc.creatorLinda, H
dc.creatorCullheim, S
dc.date2004
dc.dateDEC 21
dc.date2014-11-17T06:31:34Z
dc.date2015-11-26T16:39:57Z
dc.date2014-11-17T06:31:34Z
dc.date2015-11-26T16:39:57Z
dc.date.accessioned2018-03-28T23:23:42Z
dc.date.available2018-03-28T23:23:42Z
dc.identifierProceedings Of The National Academy Of Sciences Of The United States Of America. Natl Acad Sciences, v. 101, n. 51, n. 17843, n. 17848, 2004.
dc.identifier0027-8424
dc.identifierWOS:000225951500050
dc.identifier10.1073/pnas.0408154101
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/53714
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/53714
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/53714
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1272609
dc.descriptionRecently, MHC class I molecules have been shown to be important for the retraction of synaptic connections that normally occurs during development [Huh, G.S., Boulanger, L. M., Du, H., Riquelme, P. A., Brotz, T. M. & Shatz, C. J. (2000) Science 290, 2155-2158]. In the adult CNS, a classical response of neurons to axon lesion is the detachment of synapses from the cell body and dendrites. We have investigated whether MHC I molecules are involved also in this type of synaptic detachment by studying the synaptic input to sciatic motoneurons at 1 week after peripheral nerve transection in beta2-microglobulin or transporter associated with antigen processing 1-null mutant mice, in which cell surface MHC I expression is impaired. Surprisingly, lesioned motoneurons in mutant mice showed more extensive synaptic detachments than those in wildtype animals. This surplus removal of synapses was entirely directed toward inhibitory synapses assembled in clusters. In parallel, a significantly smaller population of motoneurons reinnervated the distal stump of the transected sciatic nerve in mutants. MHC I molecules, which traditionally have been linked with immunological mechanisms, are thus crucial for a selective maintenance of synapses during the synaptic removal process in neurons after lesion, and the lack of MHC I expression may impede the ability of neurons to regenerate axons.
dc.description101
dc.description51
dc.description17843
dc.description17848
dc.languageen
dc.publisherNatl Acad Sciences
dc.publisherWashington
dc.publisherEUA
dc.relationProceedings Of The National Academy Of Sciences Of The United States Of America
dc.relationProc. Natl. Acad. Sci. U. S. A.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectbeta(2)-microglobulin
dc.subjectmotoneuron
dc.subjectspinal cord
dc.subjectsynapse elimination
dc.subjectnerve lesion
dc.subjectCentral-nervous-system
dc.subjectT-cells
dc.subjectIntramedullary Axotomy
dc.subjectQuantitative-analysis
dc.subjectHypoglossal Nucleus
dc.subjectSpinal Motoneurons
dc.subjectAdult Cat
dc.subjectExpression
dc.subjectRat
dc.subjectDeficient
dc.titleA role for MHC class I molecules in synaptic plasticity and regeneration of neurons after axotomy
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución