ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Spinal Motor Circuit Synaptic Plasticity after Peripheral Nerve Injury Depends on Microglia Activation and a CCR2 Mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 51 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Dual Role of Microglial TREM2 in Neuronal Degeneration and Regeneration After Axotomy.bioRxiv : the preprint server for biology · 2026Article
- Targeting Glutamate Excitotoxicity With Memantine Modulates Glial Response and Protects Motoneurons After Spinal Root Lesion.Journal of neurochemistry · 2026Article
- Changes in Spinal Neural Circuit Plasticity in a Rat Sciatic Nerve Transection Model.Brain and behavior · 2026Article
- Electrical Stimulation and Platelet-Rich Plasma as Complementary Approaches for Peripheral Nerve Regeneration.Cellular and molecular neurobiology · 2025Review
- Is TREM2 a Stretch: Implications of TREM2 Along Spinal Cord Circuits in Health, Aging, Injury, and Disease.Cells · 2025Review
- Defined human tri-lineage brain microtissues.bioRxiv : the preprint server for biology · 2025Article
- Effect of microglial Pd1 on glial scar formation after spinal cord injury in mice.The Journal of biological chemistry · 2025Article
- Region-specific response of central microglial cells to sciatic nerve demyelination through sensory and motor pathways.Histology and histopathology · 2024Article
- Modulation of central synapse remodeling after remote peripheral injuries by the CCL2-CCR2 axis and microglia.Cell reports · 2024Article
- DLK signaling in axotomized neurons triggers complement activation and loss of upstream synapses.Cell reports · 2024Article
- Extracellular vesicles set the stage for brain plasticity and recovery by multimodal signalling.Brain : a journal of neurology · 2024Review
- Effects of local and systemic treatment with human natural killer-1 mimetic peptide (HNK-1) after ventral root avulsion and reimplantation in mice.The journal of venomous animals and toxins including tropical diseases · 2024Article
- Article
- Temporal changes of spinal microglia in murine models of neuropathic pain: a scoping review.Frontiers in immunology · 2024Article
- SnRNA-seq reveals the heterogeneity of spinal ventral horn and mechanism of motor neuron axon regeneration.iScience · 2023Article
- 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
- Celsr2 Knockout Alleviates Inhibitory Synaptic Stripping and Benefits Motoneuron Survival and Axon Regeneration After Branchial Plexus Avulsion.Molecular neurobiology · 2023Article
- Article
- Accumulation of misfolded SOD1 outlines distinct patterns of motor neuron pathology and death during disease progression in a SOD1Brain pathology (Zurich, Switzerland) · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Peripheral nerve injury results in persistent motor deficits, even after the nerve regenerates and muscles are reinnervated. This lack of functional recovery is partly explained by brain and spinal cord circuit alterations triggered by the injury, but the mechanisms are generally unknown. One example of this plasticity is the die-back in the spinal cord ventral horn of the projections of proprioceptive axons mediating the stretch reflex (Ia afferents). Consequently, Ia information about muscle length and dynamics is lost from ventral spinal circuits, degrading motor performance after nerve regeneration. Simultaneously, there is activation of microglia around the central projections of peripherally injured Ia afferents, suggesting a possible causal relationship between neuroinflammation and Ia axon removal. Therefore, we used mice (both sexes) that allow visualization of microglia (CX3CR1-GFP) and infiltrating peripheral myeloid cells (CCR2-RFP) and related changes in these cells to Ia synaptic losses (identified by VGLUT1 content) on retrogradely labeled motoneurons. Microgliosis around axotomized motoneurons starts and peaks within 2 weeks after nerve transection. Thereafter, this region becomes infiltrated by CCR2 cells, and VGLUT1 synapses are lost in parallel. Immunohistochemistry, flow cytometry, and genetic lineage tracing showed that infiltrating CCR2 cells include T cells, dendritic cells, and monocytes, the latter differentiating into tissue macrophages. VGLUT1 synapses were rescued after attenuating the ventral microglial reaction by removal of colony stimulating factor 1 from motoneurons or in CCR2 global KOs. Thus, both activation of ventral microglia and a CCR2-dependent mechanism are necessary for removal of VGLUT1 synapses and alterations in Ia-circuit function following nerve injuries.
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