ArticleeNeuro
AMPA Receptor Phosphorylation and Synaptic Colocalization on Motor Neurons Drive Maladaptive Plasticity below Complete Spinal Cord Injury.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- [Orexin-A promotes motor function recovery of rats with spinal cord injury by regulating ionotropic glutamate receptors].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Disuse plasticity limits spinal cord injury recovery.iScience · 2025Article
- Pathophysiologic Mechanisms of Severe Spinal Cord Injury and Neuroplasticity Following Decompressive Laminectomy and Expansive Duraplasty: A Systematic Review.Neurology international · 2025Review
- Improving rigor and reproducibility in western blot experiments with the blotRig analysis.Scientific reports · 2024Article
- Updating perspectives on spinal cord function: motor coordination, timing, relational processing, and memory below the brain.Frontiers in systems neuroscience · 2024Review
- Green Light Exposure Elicits Anti-inflammation, Endogenous Opioid Release and Dampens Synaptic Potentiation to Relieve Post-surgical Pain.The journal of pain · 2023Article
- Behavioral studies of spinal conditioning: The spinal cord is smarter than you think it is.Journal of experimental psychology. Animal learning and cognition · 2022Article
- Ionic Plasticity: Common Mechanistic Underpinnings of Pathology in Spinal Cord Injury and the Brain.Cells · 2022Review
- Review
- Noxious Stimulation Induces Acute Hemorrhage and Impairs Long-Term Recovery after Spinal Cord Injury (SCI) in Female Rats: Evidence Estrous Cycle May Have a Modulatory Effect.Neurotrauma reports · 2022Article
- Debunking a myth: plant consciousness.Protoplasma · 2021Review
- Machine intelligence identifies soluble TNFa as a therapeutic target for spinal cord injury.Scientific reports · 2021Article
- Learning to promote recovery after spinal cord injury.Experimental neurology · 2020Review
- A brief period of moderate noxious stimulation induces hemorrhage and impairs locomotor recovery after spinal cord injury.Physiology & behavior · 2019Article
- Preferential generation of CaThe Journal of biological chemistry · 2019Article
- Article
- Engaging pain fibers after a spinal cord injury fosters hemorrhage and expands the area of secondary injury.Experimental neurology · 2019Article
- Metaplasticity within the spinal cord: Evidence brain-derived neurotrophic factor (BDNF), tumor necrosis factor (TNF), and alterations in GABA function (ionic plasticity) modulate pain and the capacity to learn.Neurobiology of learning and memory · 2018Article
- Fasudil Enhances Therapeutic Efficacy of Neural Stem Cells in the Mouse Model of MPTP-Induced Parkinson's Disease.Molecular neurobiology · 2017Article
- Neurotrophic factor and Trk signaling mechanisms underlying the promotion of motor recovery after acute spinal cord injury in rats.Experimental and therapeutic medicine · 2017Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Clinical spinal cord injury (SCI) is accompanied by comorbid peripheral injury in 47% of patients. Human and animal modeling data have shown that painful peripheral injuries undermine long-term recovery of locomotion through unknown mechanisms. Peripheral nociceptive stimuli induce maladaptive synaptic plasticity in dorsal horn sensory systems through AMPA receptor (AMPAR) phosphorylation and trafficking to synapses. Here we test whether ventral horn motor neurons in rats demonstrate similar experience-dependent maladaptive plasticity below a complete SCI in vivo. Quantitative biochemistry demonstrated that intermittent nociceptive stimulation (INS) rapidly and selectively increases AMPAR subunit GluA1 serine 831 phosphorylation and localization to synapses in the injured spinal cord, while reducing synaptic GluA2. These changes predict motor dysfunction in the absence of cell death signaling, suggesting an opportunity for therapeutic reversal. Automated confocal time-course analysis of lumbar ventral horn motor neurons confirmed a time-dependent increase in synaptic GluA1 with concurrent decrease in synaptic GluA2. Optical fractionation of neuronal plasma membranes revealed GluA2 removal from extrasynaptic sites on motor neurons early after INS followed by removal from synapses 2 h later. As GluA2-lacking AMPARs are canonical calcium-permeable AMPARs (CP-AMPARs), their stimulus- and time-dependent insertion provides a therapeutic target for limiting calcium-dependent dynamic maladaptive plasticity after SCI. Confirming this, a selective CP-AMPAR antagonist protected against INS-induced maladaptive spinal plasticity, restoring adaptive motor responses on a sensorimotor spinal training task. These findings highlight the critical involvement of AMPARs in experience-dependent spinal cord plasticity after injury and provide a pharmacologically targetable synaptic mechanism by which early postinjury experience shapes motor plasticity.
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