MHC class I upregulation is not sufficient to rescue neonatal alpha motoneurons after peripheral axotomy

dc.creatorPayes, ACLM
dc.creatorZanon, RG
dc.creatorPierucci, A
dc.creatorOliveira, ALR
dc.date2008
dc.dateOCT 31
dc.date2014-07-30T14:01:38Z
dc.date2015-11-26T16:07:00Z
dc.date2014-07-30T14:01:38Z
dc.date2015-11-26T16:07:00Z
dc.date.accessioned2018-03-28T22:55:48Z
dc.date.available2018-03-28T22:55:48Z
dc.identifierBrain Research. Elsevier Science Bv, v. 1238, n. 23, n. 30, 2008.
dc.identifier0006-8993
dc.identifierWOS:000260858100003
dc.identifier10.1016/j.brainres.2008.08.032
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/56659
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/56659
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1266053
dc.descriptionAssociated with neuronal death, profound synaptic changes occur in the spinal cord during the apoptotic process triggered after axotomy in neonatal rats. With respect to this, the major histocompatibility complex of class I (MHC class I) has recently emerged as a new mechanism related to synaptic stripping and plasticity. The present study investigated the impact of upregulating MHC class I expression by treatment with beta interferon (beta INF) on motoneuron survival, synaptic plasticity and astrogliosis after neonatal sciatic nerve injury. P2 rats were subjected to unilateral axotomy followed by three days of beta INF treatment. The results were analyzed by counting Nissl stained motoneurons, immunohistochemistry (anti-synaptophysin, MHC class I, GFAP and lba-1) and transmission electron microscopy, INF treatment induced an increased expression of MHC class 1, which resulted in a stronger synaptic elimination process in the spinal cord, as seen by the synaptophysin labeling. GFAP and lba-1 upregulation were not significantly altered by the INF, treatment, displaying the same degree of enhanced reactivity as compared to the placebo group, The ultrastructural analysis showed that, apart from the overall reduction of inputs in the neuropil, no statistical differences were present when comparing the INF and placebo treated animals. Also, neuronal survival was not altered by cytokine administration. The present results provide evidence that MHC class I upregulation after neonatal injury does not change the fate of lesioned motoneurons. In this way, the lack of neurotrophic support may cause broader synaptic loss, which superposes the more subtle effects of the upregulation of MHC class I. (C) 2008 Elsevier B.V. All rights reserved.
dc.description1238
dc.description23
dc.description30
dc.languageen
dc.publisherElsevier Science Bv
dc.publisherAmsterdam
dc.publisherHolanda
dc.relationBrain Research
dc.relationBrain Res.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectCytokine
dc.subjectMotoneuron
dc.subjectNeonatal
dc.subjectAxotomy
dc.subjectMHC class I
dc.subjectSynaptic Plasticity
dc.subjectSpinal Motoneurons
dc.subjectRat Motoneurons
dc.subjectExpression
dc.subjectTerminals
dc.subjectResponses
dc.subjectLesions
dc.subjectGap-43
dc.subjectCord
dc.subjectCns
dc.titleMHC class I upregulation is not sufficient to rescue neonatal alpha motoneurons after peripheral axotomy
dc.typeArtículos de revistas


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