ArticleNeuron2022
Spinal cord retinoic acid receptor signaling gates mechanical hypersensitivity in neuropathic pain.
Article in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 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
- Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026Review
- Article
- Treatment of spinal cord injury, by restoration of neuronal networks using a combination of surgery and KCL-286, an orally available retinoic acid receptor β drug.Frontiers in surgery · 2026Review
- Energy Metabolism and Cancer Pain: A Pathway to Innovative Treatment Strategies.Current topics in medicinal chemistry · 2026Review
- Article
- Stage-specific transcriptomic alterations in the spinal cord reveal key regulatory genes and potential therapeutic targets in a rat model of neuropathic pain.Journal of translational medicine · 2025Article
- Cingulate retinoic acid signaling regulates neuropathic pain and comorbid anxiodepression via extracellular matrix homeostasis.The Journal of clinical investigation · 2025Article
- Neuropathic Pain-Like Responses in a Chronic CNS Injury Model Are Mediated by Corticospinal-Targeted Spinal Interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Retinoic acid-mediated homeostatic plasticity drives cell type-specific CP-AMPAR accumulation in nucleus accumbens core and incubation of cocaine craving.Molecular psychiatry · 2025Article
- Article
- Targeting spinal mechanistic target of rapamycin complex 2 alleviates inflammatory and neuropathic pain.Brain : a journal of neurology · 2025Article
- Differential Neuronal Activation of Nociceptive Pathways in Neuropathic Pain After Spinal Cord Injury.Cellular and molecular neurobiology · 2025Article
- Opioidergic activation of the descending pain inhibitory system underlies placebo analgesia.Science advances · 2025Article
- Establishment of a Magnetically Controlled Scalable Nerve Injury Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Retinoic acid-mediated homeostatic plasticity in the nucleus accumbens core contributes to incubation of cocaine craving.Psychopharmacology · 2024Article
- Parvalbumin gates chronic pain through the modulation of firing patterns in inhibitory neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Parabrachial Calca neurons drive nociplasticity.Cell reports · 2024Article
- Nerve injury disrupts temporal processing in the spinal cord dorsal horn through alterations in PVCell reports · 2024Article
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3 authors at 3 institutions in 1 country.
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Abstract
Central sensitization caused by spinal disinhibition is a key mechanism of mechanical allodynia in neuropathic pain. However, the molecular mechanisms underlying spinal disinhibition after nerve injury remain unclear. Here, we show in mice that spared nerve injury (SNI), which induces mechanical hypersensitivity and neuropathic pain, triggers homeostatic reduction of inhibitory outputs from dorsal horn parvalbumin-positive (PV+) interneurons onto both primary afferent terminals and excitatory interneurons. The reduction in inhibitory outputs drives hyperactivation of the spinal cord nociceptive pathway, causing mechanical hypersensitivity. We identified the retinoic acid receptor RARα, a central regulator of homeostatic plasticity, as the key molecular mediator for this synaptic disinhibition. Deletion of RARα in spinal PV+ neurons or application of an RARα antagonist in the spinal cord prevented the development of SNI-induced mechanical hypersensitivity. Our results identify RARα as a crucial molecular effector for neuropathic pain and a potential target for its treatment.
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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.