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Impact of acute inflammation on spinal motoneuron synaptic plasticity following ventral root avulsion

DOI: 10.1186/1742-2094-7-29

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Lewis rats were subjected to unilateral avulsion of lumbar ventral roots (VRA) and divided into three groups: VRA control, VRA at peak of EAE, and VRA during EAE remission. The animals were sacrificed and their lumbar spinal cords processed for immunohistochemistry, transmission electron microscopy, and motoneuron counting.The results indicate a reduction in astroglial reaction, a maintenance of microglial reactivity, and increases in synaptic covering of, and survival of, motoneurons in the VRA+EAE group as compared to VRA alone.The present findings indicate that CNS inflammation may directly influence synaptic plasticity as well as the stability of neuronal networks, positively influencing the survival of lesioned neurons.Traumatic lesions to the spinal cord, which involve neuronal death, convey devastating and permanent loss of function. Alterations also develop in response to the consequent local hemorrhage and ischemia [1]. Among these alterations, upregulation of receptors for neurotrophic factors such as the low affinity neurotrophin receptor p75NTR [2], the high affinity trkB receptor for BDNF [3], and the GFRa-1 receptor for glial derived neurotrophic factor (GDNF) [4], are well established examples. Additionally, upregulation of proteins such as growth associated protein-43 (GAP-43) [5,6] and calcitonin gene-related peptide (CGRP), and down-regulation of receptors and enzymes involved in neurotransmission, including choline acetyltransferase (ChAT) and NMDA receptors [6], may be cited as important responses to injury that are related to a regenerative strategy [5-8] in the cell body.In adults, such a physiological shift is more related to cell repair than to survival [8]. However, lesions close to the surface of the spinal cord may result in extensive degeneration of adult motoneurons, as is the case after avulsion of ventral roots (VRA), an experimental model used to investigate adult neuronal degeneration [6,9,10]. Koliatsos et al. [9] have demonstrated

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