ArticleMolecular pain2014
Spinal 5-HT3 receptors mediate descending facilitation and contribute to behavioral hypersensitivity via a reciprocal neuron-glial signaling cascade.
Article in Molecular pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Pooled it
- Efficacy of azasetron on postoperative chronic pain after pulmonary surgery: a randomized triple-blind controlled trial.BMC anesthesiology · 2024Trial
- Review
- The Informational Blackout chronic pain and fatigue as rational outputs of a brain operating on degraded biological signals.Frontiers in pain research (Lausanne, Switzerland) · 2026Article
- Centralizing the Knowledge and Interpretation of Pain in Chemotherapy-Induced Peripheral Neuropathy: A Paradigm Shift towards Brain-Centric Approaches.Brain sciences · 2024Review
- Evaluation of the effect of intraoperative tropisetron on postoperative rebound pain after brachial plexus block: a randomized controlled trial.Pain reports · 2024Article
- Descending serotonergic modulation from rostral ventromedial medulla to spinal trigeminal nucleus is involved in experimental occlusal interference-induced chronic orofacial hyperalgesia.The journal of headache and pain · 2023Article
- Imbalance in the spinal serotonergic pathway induces aggravation of mechanical allodynia and microglial activation in carrageenan inflammation.The Korean journal of pain · 2023Article
- A model for irritable bowel syndrome and anxiety comorbidities in relation to alcohol use disorders.Frontiers in medicine · 2023Article
- Spinal CCK1 Receptors Contribute to Somatic Pain Hypersensitivity Induced by Malocclusion via a Reciprocal Neuron-Glial Signaling Cascade.The journal of pain · 2022Article
- SAHA Inhibits Somatic Hyperalgesia Induced by Stress Combined with Orofacial Inflammation Through Targeting Different Spinal 5-HT Receptor Subtypes.Neurochemical research · 2022Article
- Review
- NMDARs mediate peripheral and central sensitization contributing to chronic orofacial pain.Frontiers in cellular neuroscience · 2022Review
- Effect of Bufalin-PLGA Microspheres in the Alleviation of Neuropathic PainFrontiers in pharmacology · 2022Article
- Evaluation of the Effect of Vortioxetine on Pain Threshold By Hot-Plate Test in Mice.Noro psikiyatri arsivi · 2021Article
- Monoaminergic and Opioidergic Modulation of Brainstem Circuits: New Insights Into the Clinical Challenges of Pain Treatment?Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Contribution of central sensitization to stress-induced spreading hyperalgesia in rats with orofacial inflammation.Molecular brain · 2020Article
- Mild Traumatic Brain Injury Causes Nociceptive Sensitization through Spinal Chemokine Upregulation.Scientific reports · 2019Article
- Pathological pain processing in mouse models of multiple sclerosis and spinal cord injury: contribution of plasma membrane calcium ATPase 2 (PMCA2).Journal of neuroinflammation · 2019Article
- Enhanced descending pain facilitation in acute traumatic brain injury.Experimental neurology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundIt has been recently recognized that the descending serotonin (5-HT) system from the rostral ventromedial medulla (RVM) in the brainstem and the 5-HT3 receptor subtype in the spinal dorsal horn are involved in enhanced descending pain facilitation after tissue and nerve injury. However, the mechanisms underlying the activation of the 5-HT3 receptor and its contribution to facilitation of pain remain unclear.
resultsIn the present study, activation of spinal 5-HT3 receptors by intrathecal injection of a selective 5-HT3 receptor agonist SR 57227 induced spinal glial hyperactivity, neuronal hyperexcitability and pain hypersensitivity in rats. We found that there was neuron-to-microglia signaling via the chemokine fractalkine, microglia to astrocyte signaling via cytokine IL-18, astrocyte to neuronal signaling by IL-1β, and enhanced activation of NMDA receptors in the spinal dorsal horn. Glial hyperactivation in spinal dorsal horn after hindpaw inflammation was also attenuated by molecular depletion of the descending 5-HT system by intra-RVM Tph-2 shRNA interference.
conclusionsThese findings offer new insights into the cellular and molecular mechanisms at the spinal level responsible for descending 5-HT-mediated pain facilitation during the development of persistent pain after tissue and nerve injury. New pain therapies should focus on prime targets of descending facilitation-induced glial involvement, and in particular the blocking of intercellular signaling transduction between neurons and glia.
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