ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Group I metabotropic glutamate receptors control metaplasticity of spinal cord learning through a protein kinase C-dependent mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
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- 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
- Brain-Dependent Processes Fuel Pain-Induced Hemorrhage After Spinal Cord Injury.Frontiers in systems neuroscience · 2019Article
- The Spinal Cord, Not to Be Forgotten: the Final Common Path for Development, Training and Recovery of Motor Function.Perspectives on behavior science · 2018Article
- Spinal activation of protein kinase C elicits phrenic motor facilitation.Respiratory physiology & neurobiology · 2018Article
- 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
- Immunoexcitotoxicity as the central mechanism of etiopathology and treatment of autism spectrum disorders: A possible role of fluoride and aluminum.Surgical neurology international · 2018Review
- What Is Being Trained? How Divergent Forms of Plasticity Compete To Shape Locomotor Recovery after Spinal Cord Injury.Journal of neurotrauma · 2017Review
- Sparing of Descending Axons Rescues Interneuron Plasticity in the Lumbar Cord to Allow Adaptive Learning After Thoracic Spinal Cord Injury.Frontiers in neural circuits · 2016Article
- Phrenic long-term facilitation requires PKCθ activity within phrenic motor neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- The association between spinal cord trauma-sensitive miRNAs and pain sensitivity, and their regulation by morphine.Neurochemistry international · 2014Article
- Metaplasticity and behavior: how training and inflammation affect plastic potential within the spinal cord and recovery after injury.Frontiers in neural circuits · 2014Review
- Regulatory effects of intermittent noxious stimulation on spinal cord injury-sensitive microRNAs and their presumptive targets following spinal cord contusion.Frontiers in neural circuits · 2014Article
- AMPA receptor mediated behavioral plasticity in the isolated rat spinal cord.Behavioural brain research · 2013Article
- Temporal regularity determines the impact of electrical stimulation on tactile reactivity and response to capsaicin in spinally transected rats.Neuroscience · 2012Article
- Spinal atypical protein kinase C activity is necessary to stabilize inactivity-induced phrenic motor facilitation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Time-dependent cross talk between spinal serotonin 5-HT2A receptor and mGluR1 subserves spinal hyperexcitability and neuropathic pain after nerve injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Brain-derived neurotrophic factor promotes adaptive plasticity within the spinal cord and mediates the beneficial effects of controllable stimulation.Neuroscience · 2012Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Neurons within the spinal cord can support several forms of plasticity, including response-outcome (instrumental) learning. After a complete spinal transection, experimental subjects are capable of learning to hold the hindlimb in a flexed position (response) if shock (outcome) is delivered to the tibialis anterior muscle when the limb is extended. This response-contingent shock produces a robust learning that is mediated by ionotropic glutamate receptors (iGluRs). Exposure to nociceptive stimuli that are independent of limb position (e.g., uncontrollable shock; peripheral inflammation) produces a long-term (>24 h) inhibition of spinal learning. This inhibition of plasticity in spinal learning is itself a form of plasticity that requires iGluR activation and protein synthesis. Plasticity of plasticity (metaplasticity) in the CNS has been linked to group I metabotropic glutamate receptors (subtypes mGluR1 and mGluR5) and activation of protein kinase C (PKC). The present study explores the role of mGluRs and PKC in the metaplastic inhibition of spinal cord learning using a combination of behavioral, pharmacological, and biochemical techniques. Activation of group I mGluRs was found to be both necessary and sufficient for metaplastic inhibition of spinal learning. PKC was activated by stimuli that inhibit spinal learning, and inhibiting PKC activity restored the capacity for spinal learning. Finally, a PKC inhibitor blocked the metaplastic inhibition of spinal learning produced by a group I mGluR agonist. The data strongly suggest that group I mGluRs control metaplasticity of spinal learning through a PKC-dependent mechanism, providing a potential therapeutic target for promoting use-dependent plasticity 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.