ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Induction of thermal hyperalgesia and synaptic long-term potentiation in the spinal cord lamina I by TNF-α and IL-1β is mediated by glial cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.
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Who cites it
123 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Cannabinoid CB1 Receptor Regulates Spinal Dorsal Horn Synaptic Plasticity in a Mouse Model of Neuropathic Pain through the CB1R/SREBP1/NAMPT/SIRT1 Metabolic Regulatory Framework.Brain and behavior · 2026Article
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- The actions of morphine on microglia and the underlying effects on associated adverse effects.Psychopharmacology · 2026Review
- Potential mechanisms of the glucocorticoid withdrawal syndrome.European journal of endocrinology · 2026Review
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- Astrocyte Regulation of Spinal Circuit Function.Journal of neurochemistry · 2026Review
- From multi-target mechanisms to clinical translation: the analgesic potential of quercetin.Frontiers in pharmacology · 2026Review
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- Astrogliopathology: A core pathogenic factor in diabetic neuropathic pain.IBRO neuroscience reports · 2025Review
- AAV-mediated STC-1 expression mitigates neuroinflammation and preserves visual function in degenerative retinopathy.Journal of translational medicine · 2025Article
- 4E-BP1-dependent translation in microglia controls mechanical hypersensitivity in male and female mice.The Journal of clinical investigation · 2025Article
- How microglia contribute to the induction and maintenance of neuropathic pain.Nature reviews. Neuroscience · 2025Review
- Mechanisms of Remifentanil-Induced Postoperative Hyperalgesia: A Comprehensive Review.Drug design, development and therapy · 2025Review
- Spinal cord stimulation using time-dynamic pulses achieves longer reversal of allodynia compared to tonic pulses in a rat model of neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
- Is It Time to Revisit the Role of Interleukin-1 Inhibitors in Osteoarthritis?Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Pharmacological Network Analysis of the Functions and Mechanism of Quercetin From Jisuikang (JSK) in Spinal Cord Injury (SCI).Journal of cellular and molecular medicine · 2024Article
- Role of Exercise on Inflammation Cytokines of Neuropathic Pain in Animal Models.Molecular neurobiology · 2024Review
- Analgesic Effect of Human Placenta Hydrolysate on CFA-Induced Inflammatory Pain in Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Astrocyte D1/D5 Dopamine Receptors Govern Non-Hebbian Long-Term Potentiation at Sensory Synapses onto Lamina I Spinoparabrachial Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
63 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term potentiation (LTP) of synaptic strength in nociceptive pathways is a cellular model of hyperalgesia. The emerging literature suggests a role for cytokines released by spinal glial cells for both LTP and hyperalgesia. However, the underlying mechanisms are still not fully understood. In rat lumbar spinal cord slices, we now demonstrate that conditioning high-frequency stimulation of primary afferents activated spinal microglia within <30 min and spinal astrocytes within ~2 s. Activation of spinal glia was indispensible for LTP induction at C-fiber synapses with spinal lamina I neurons. The cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), which are both released by activated glial cells, were individually sufficient and necessary for LTP induction via redundant pathways. They differentially amplified 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl)-propanoic acid receptor-mediated and N-methyl-D-aspartic acid receptor-mediated synaptic currents in lamina I neurons. Unexpectedly, the synaptic effects by IL-1β and TNF-α were not mediated directly via activation of neuronal cytokine receptors, but rather, indirectly via IL-1 receptors and TNF receptors being expressed on glial cells in superficial spinal dorsal horn. Bath application of IL-1β or TNF-α led to the release profiles of pro-inflammatory and anti-inflammatory cytokines, chemokines, and growth factors, which overlapped only partially. Heat hyperalgesia induced by spinal application of either IL-1β or TNF-α in naive animals also required activation of spinal glial cells. These results reveal a novel, decisive role of spinal glial cells for the synaptic effects of IL-1β and TNF-α and for some forms of hyperalgesia.
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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.