ArticlePloS one2012
Glial tumor necrosis factor alpha (TNFα) generates metaplastic inhibition of spinal learning.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
39 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- Updating perspectives on spinal cord function: motor coordination, timing, relational processing, and memory below the brain.Frontiers in systems neuroscience · 2024Review
- 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
- 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
- Locomotor deficits induced by lumbar muscle inflammation involve spinal microglia and are independent of KCC2 expression in a mouse model of complete spinal transection.Experimental neurology · 2021Article
- Machine intelligence identifies soluble TNFa as a therapeutic target for spinal cord injury.Scientific reports · 2021Article
- Evidence That the Central Nervous System Can Induce a Modification at the Neuromuscular Junction That Contributes to the Maintenance of a Behavioral Response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- 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
- Peripheral Inflammation Accelerates the Onset of Mechanical Hypersensitivity after Spinal Cord Injury and Engages Tumor Necrosis Factor α Signaling Mechanisms.Journal of neurotrauma · 2019Article
- Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2018Review
- 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
- TRAF3IP2, a novel therapeutic target in glioblastoma multiforme.Oncotarget · 2018Article
- Pain Input After Spinal Cord Injury (SCI) Undermines Long-Term Recovery and Engages Signal Pathways That Promote Cell Death.Frontiers in systems neuroscience · 2018Article
- What Is Being Trained? How Divergent Forms of Plasticity Compete To Shape Locomotor Recovery after Spinal Cord Injury.Journal of neurotrauma · 2017Review
- When Pain Hurts: Nociceptive Stimulation Induces a State of Maladaptive Plasticity and Impairs Recovery after Spinal Cord Injury.Journal of neurotrauma · 2017Review
- Acute spinal cord injury (SCI) transforms how GABA affects nociceptive sensitization.Experimental neurology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Injury-induced overexpression of tumor necrosis factor alpha (TNFα) in the spinal cord can induce chronic neuroinflammation and excitotoxicity that ultimately undermines functional recovery. Here we investigate how TNFα might also act to upset spinal function by modulating spinal plasticity. Using a model of instrumental learning in the injured spinal cord, we have previously shown that peripheral intermittent stimulation can produce a plastic change in spinal plasticity (metaplasticity), resulting in the prolonged inhibition of spinal learning. We hypothesized that spinal metaplasticity may be mediated by TNFα. We found that intermittent stimulation increased protein levels in the spinal cord. Using intrathecal pharmacological manipulations, we showed TNFα to be both necessary and sufficient for the long-term inhibition of a spinal instrumental learning task. These effects were found to be dependent on glial production of TNFα and involved downstream alterations in calcium-permeable AMPA receptors. These findings suggest a crucial role for glial TNFα in undermining spinal learning, and demonstrate the therapeutic potential of inhibiting TNFα activity to rescue and restore adaptive spinal plasticity to the injured spinal cord. TNFα modulation represents a novel therapeutic target for improving rehabilitation after spinal cord injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.