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Type: Artigo de periódico
Title: Synaptic Rearrangement Following Axonal Injury: Old And New Players
Author: Spejo
Aline Barroso; Oliveira
Alexandre L. R.
Abstract: Following 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.
Subject: Spinal-cord-injury
Ventral Root Avulsion
Toll-like Receptors
Mhc Class-i
Nogo-a Antibody
Sciatic-nerve Transection
Fibrillary Acidic Protein
Mesenchymal Stem-cells
Chondroitin Sulfate Proteoglycans
Myelin-associated Glycoprotein
Country: OXFORD
Rights: embargo
Identifier DOI: 10.1016/j.neuropharm.2014.11.002
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

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