ArticlePloS one2013
The extent of synaptic stripping of motoneurons after axotomy is not correlated to activation of surrounding glia or downregulation of postsynaptic adhesion molecules.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Dual Role of Microglial TREM2 in Neuronal Degeneration and Regeneration After Axotomy.bioRxiv : the preprint server for biology · 2026Article
- Structural Preservation Does Not Ensure Function at Sensory Ia-Motoneuron Synapses following Peripheral Nerve Injury and Repair.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- The Role of Microglia in Neuroinflammation of the Spinal Cord after Peripheral Nerve Injury.Cells · 2022Review
- VEGF is an essential retrograde trophic factor for motoneurons.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- CD4+ T cell expression of the IL-10 receptor is necessary for facial motoneuron survival after axotomy.Journal of neuroinflammation · 2020Article
- Synaptic Plasticity on Motoneurons After Axotomy: A Necessary Change in Paradigm.Frontiers in molecular neuroscience · 2020Review
- Spinal Motor Circuit Synaptic Plasticity after Peripheral Nerve Injury Depends on Microglia Activation and a CCR2 Mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Origins of Phantom Limb Pain.Molecular neurobiology · 2018Review
- MHCI promotes developmental synapse elimination and aging-related synapse loss at the vertebrate neuromuscular junction.Brain, behavior, and immunity · 2016Article
- Synapse Formation in Monosynaptic Sensory-Motor Connections Is Regulated by Presynaptic Rho GTPase Cdc42.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Neuronal BDNF signaling is necessary for the effects of treadmill exercise on synaptic stripping of axotomized motoneurons.Neural plasticity · 2015Article
- Psychiatric disturbances regulate the innate immune system in CSF of conscious mice.Translational psychiatry · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synapse elimination in the adult central nervous system can be modelled by axotomy of spinal motoneurons which triggers removal of synapses from the cell surface of lesioned motoneurons by processes that remain elusive. Proposed candidate mechanisms are removal of synapses by reactive microglia and astrocytes, based on the remarkable activation of these cell types in the vicinity of motoneurons following axon lesion, and/or decreased expression of synaptic adhesion molecules in lesioned motoneurons. In the present study, we investigated glia activation and adhesion molecule expression in motoneurons in two mouse strains with deviant patterns of synapse elimination following axotomy. Mice deficient in complement protein C3 display a markedly reduced loss of synapses from axotomized motoneurons, whereas mice with impaired function of major histocompatibility complex (MHC) class Ia display an augmented degree of stripping after axotomy. Activation of microglia and astrocytes was assessed by semiquantative immunohistochemistry for Iba 1 (microglia) and GFAP (astrocytes), while expression of synaptic adhesion molecules was determined by in situ hybridization. In spite of the fact that the two mouse strains display very different degrees of synapse elimination, no differences in terms of glial activation or in the downregulation of the studied adhesion molecules (SynCAM1, neuroligin-2,-3 and netrin G-2 ligand) could be detected. We conclude that neither glia activation nor downregulation of synaptic adhesion molecules are correlated to the different extent of the synaptic stripping in the two studied strains. Instead the magnitude of the stripping event is most likely a consequence of a precise molecular signaling, which at least in part is mediated by immune molecules.
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