Synaptic Rearrangement Following Axonal Injury: Old And New Players

dc.creatorSpejo
dc.creatorAline Barroso; Oliveira
dc.creatorAlexandre L. R.
dc.date2015-SEP
dc.date2016-06-07T13:21:12Z
dc.date2016-06-07T13:21:12Z
dc.date.accessioned2018-03-29T01:41:05Z
dc.date.available2018-03-29T01:41:05Z
dc.identifier
dc.identifierSynaptic Rearrangement Following Axonal Injury: Old And New Players. Pergamon-elsevier Science Ltd, v. 96, p. 113-123 SEP-2015.
dc.identifier0028-3908
dc.identifierWOS:000358103800012
dc.identifier10.1016/j.neuropharm.2014.11.002
dc.identifierhttp://www.sciencedirect.com/science/article/pii/S0028390814004055
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/243042
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1306740
dc.descriptionFollowing axotomy, the contact between motoneurons and muscle fibers is disrupted, triggering a retrograde reaction at the neuron cell body within the spinal cord. Together with chromatolysis, a hallmark of such response to injury is the elimination of presynaptic terminals apposing to the soma and proximal dendrites of the injured neuron. Excitatory inputs are preferentially eliminated, leaving the cells under an inhibitory influence during the repair process. This is particularly important to avoid glutamate excitotoxicity. Such shift from transmission to a regeneration state is also reflected by deep metabolic changes, seen by the regulation of several genes related to cell survival and axonal growth. It is unclear, however, how exactly synaptic stripping occurs, but there is substantial evidence that glial cells play an active role in this process. In one hand, immune molecules, such as the major histocompatibility complex (MHC) class I, members of the complement family and Toll-like receptors are actively involved in the elimination/reapposition of presynaptic boutons. On the other hand, plastic changes that involve sprouting might be negatively regulated by extracellular matrix proteins such as Nogo-A, MAG and scar-related chondroitin sulfate proteoglycans. Also, neurotrophins, stem cells, physical exercise and several drugs seem to improve synaptic stability, leading to functional recovery after lesion. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'. (C) 2014 Elsevier Ltd. All rights reserved.
dc.description96
dc.description
dc.description
dc.description113
dc.description123
dc.description
dc.description
dc.description
dc.languageen
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD
dc.publisher
dc.publisherOXFORD
dc.relationNEUROPHARMACOLOGY
dc.rightsembargo
dc.sourceWOS
dc.subjectSpinal-cord-injury
dc.subjectVentral Root Avulsion
dc.subjectToll-like Receptors
dc.subjectMhc Class-i
dc.subjectNogo-a Antibody
dc.subjectSciatic-nerve Transection
dc.subjectFibrillary Acidic Protein
dc.subjectMesenchymal Stem-cells
dc.subjectChondroitin Sulfate Proteoglycans
dc.subjectMyelin-associated Glycoprotein
dc.titleSynaptic Rearrangement Following Axonal Injury: Old And New Players
dc.typeArtículos de revistas
dc.typeResumo


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