ArticleProceedings of the National Academy of Sciences of the United States of America2014
Long-term potentiation of glycinergic synapses triggered by interleukin 1β.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- Targeting Spinal Dorsal Horn Sensitisation in Chronic Pain: Mechanisms and Translational Strategies.Neuroscience bulletin · 2026Review
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Nociplastic pain: the prominent role of non-neuronal cells in central and peripheral sensitization.Frontiers in immunology · 2026Review
- Identification and validation of biomarkers related to Th1 cell infiltration in neuropathic pain.Journal of inflammation (London, England) · 2023Article
- Neuropathic Pain Induces Interleukin-1β Sensitive Bimodal Glycinergic Activity in the Central Amygdala.International journal of molecular sciences · 2022Article
- Role of cathepsin K in the expression of mechanical hypersensitivity following intra-plantar inflammation.Scientific reports · 2022Article
- Glycine Receptor Subtypes and Their Roles in Nociception and Chronic Pain.Frontiers in molecular neuroscience · 2022Review
- The Role of Neuro-Immune Interactions in Chronic Pain: Implications for Clinical Practice.Journal of pain research · 2022Review
- Infusion of hESC derived Immunity-and-matrix regulatory cells improves cognitive ability in early-stage AD mice.Cell proliferation · 2021Article
- Effects of Interleukin-1β in Glycinergic Transmission at the Central Amygdala.Frontiers in pharmacology · 2021Article
- Toll-like receptor 4/nuclear factor-kappa B pathway is involved in radicular pain by encouraging spinal microglia activation and inflammatory response in a rat model of lumbar disc herniation.The Korean journal of pain · 2021Article
- Long-term potentiation of glycinergic synapses by semi-natural stimulation patterns during tonotopic map refinement.Scientific reports · 2020Article
- Astrocytes in chronic pain and itch.Nature reviews. Neuroscience · 2019Review
- Spinal αBritish journal of pharmacology · 2019Review
- Properties of neurons in the superficial laminae of trigeminal nucleus caudalis.Physiological reports · 2019Article
- Article
- Microglia in Pain: Detrimental and Protective Roles in Pathogenesis and Resolution of Pain.Neuron · 2018Review
- Long-Term Depression Induced by Optogenetically Driven Nociceptive Inputs to Trigeminal Nucleus Caudalis or Headache Triggers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Neuroinflammation and Central Sensitization in Chronic and Widespread Pain.Anesthesiology · 2018Review
- Synaptic function and plasticity in identified inhibitory inputs onto VTA dopamine neurons.The European journal of neuroscience · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Long-term potentiation (LTP) is a persistent increase in synaptic strength required for many behavioral adaptations, including learning and memory, visual and somatosensory system functional development, and drug addiction. Recent work has suggested a role for LTP-like phenomena in the processing of nociceptive information in the dorsal horn and in the generation of central sensitization during chronic pain states. Whereas LTP of glutamatergic and GABAergic synapses has been characterized throughout the central nervous system, to our knowledge there have been no reports of LTP at mammalian glycinergic synapses. Glycine receptors (GlyRs) are structurally related to GABAA receptors and have a similar inhibitory role. Here we report that in the superficial dorsal horn of the spinal cord, glycinergic synapses on inhibitory GABAergic neurons exhibit LTP, occurring rapidly after exposure to the inflammatory cytokine interleukin-1 beta. This form of LTP (GlyR LTP) results from an increase in the number and/or change in biophysical properties of postsynaptic glycine receptors. Notably, formalin-induced peripheral inflammation in vivo potentiates glycinergic synapses on dorsal horn neurons, suggesting that GlyR LTP is triggered during inflammatory peripheral injury. Our results define a previously unidentified mechanism that could disinhibit neurons transmitting nociceptive information and may represent a useful therapeutic target for the treatment of pain.
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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.