ReviewFrontiers in neural circuits2014
Metaplasticity and behavior: how training and inflammation affect plastic potential within the spinal cord and recovery after injury.
Review in Frontiers in neural circuits, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 59 citations in OpenAlex.
- Updating perspectives on spinal cord function: motor coordination, timing, relational processing, and memory below the brain.Frontiers in systems neuroscience · 2024Review
- General Anesthesia Blocks Pain-Induced Hemorrhage and Locomotor Deficits After Spinal Cord Injury in Rats.Journal of neurotrauma · 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
- Progression in translational research on spinal cord injury based on microenvironment imbalance.Bone research · 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
- 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
- Role for Physical Fitness in the Association between Age and Cognitive Function in Older Adults: A Mediation Analysis of the SABE Colombia Study.International journal of environmental research and public health · 2021Article
- Neurobiological After-Effects of Low Intensity Transcranial Electric Stimulation of the Human Nervous System: From Basic Mechanisms to Metaplasticity.Frontiers in neurology · 2021Review
- 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
- Pharmacological Transection of Brain-Spinal Cord Communication Blocks Pain-Induced Hemorrhage and Locomotor Deficits after Spinal Cord Injury in Rats.Journal of neurotrauma · 2020Article
- miR-194-5p inhibits LPS-induced astrocytes activation by directly targeting neurexophilin 1.Molecular and cellular biochemistry · 2020Article
- Learning to promote recovery after spinal cord injury.Experimental neurology · 2020Review
- Peripheral Inflammation Accelerates the Onset of Mechanical Hypersensitivity after Spinal Cord Injury and Engages Tumor Necrosis Factor α Signaling Mechanisms.Journal of neurotrauma · 2019Article
- Supraspinal Shaping of Adaptive Transitions in the State of Functional Connectivity Between Segmentally Distributed Dorsal Horn Neuronal Populations in Response to Nociception and Antinociception.Frontiers in systems neuroscience · 2019Article
- Brain-Dependent Processes Fuel Pain-Induced Hemorrhage After Spinal Cord Injury.Frontiers in systems neuroscience · 2019Article
- Impaired Motor Learning Following a Pain Episode in Intact Rats.Frontiers in 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
- The Neuroplastic and Therapeutic Potential of Spinal Interneurons in the Injured Spinal Cord.Trends in neurosciences · 2018Review
- Ionic plasticity and pain: The loss of descending serotonergic fibers after spinal cord injury transforms how GABA affects pain.Experimental neurology · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Research has shown that spinal circuits have the capacity to adapt in response to training, nociceptive stimulation and peripheral inflammation. These changes in neural function are mediated by physiological and neurochemical systems analogous to those that support plasticity within the hippocampus (e.g., long-term potentiation and the NMDA receptor). As observed in the hippocampus, engaging spinal circuits can have a lasting impact on plastic potential, enabling or inhibiting the capacity to learn. These effects are related to the concept of metaplasticity. Behavioral paradigms are described that induce metaplastic effects within the spinal cord. Uncontrollable/unpredictable stimulation, and peripheral inflammation, induce a form of maladaptive plasticity that inhibits spinal learning. Conversely, exposure to controllable or predictable stimulation engages a form of adaptive plasticity that counters these maladaptive effects and enables learning. Adaptive plasticity is tied to an up-regulation of brain derived neurotrophic factor (BDNF). Maladaptive plasticity is linked to processes that involve kappa opioids, the metabotropic glutamate (mGlu) receptor, glia, and the cytokine tumor necrosis factor (TNF). Uncontrollable nociceptive stimulation also impairs recovery after a spinal contusion injury and fosters the development of pain (allodynia). These adverse effects are related to an up-regulation of TNF and a down-regulation of BDNF and its receptor (TrkB). In the absence of injury, brain systems quell the sensitization of spinal circuits through descending serotonergic fibers and the serotonin 1A (5HT 1A) receptor. This protective effect is blocked by surgical anesthesia. Disconnected from the brain, intracellular Cl(-) concentrations increase (due to a down-regulation of the cotransporter KCC2), which causes GABA to have an excitatory effect. It is suggested that BDNF has a restorative effect because it up-regulates KCC2 and re-establishes GABA-mediated inhibition.
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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.