ArticleNature communications2016
β-arrestin-2 regulates NMDA receptor function in spinal lamina II neurons and duration of persistent pain.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 59 citations in OpenAlex.
- Noninvasive Focal Gene Delivery of Functional Neural Actuators to the Primate Spinal Cord using Focused Ultrasound.bioRxiv : the preprint server for biology · 2026Article
- SIGMAR1 Drives the Development of Neuropathic Pain by Promoting AMPA Receptor Membrane Trafficking Through Interacting with NPTX1 in Male Mice.Neuroscience bulletin · 2026Article
- Time-Restricted Feeding Alters Behavior in a Sex-Specific Manner in Mice With Neuropathic Pain.Molecular nutrition & food research · 2026Article
- Discovery of a β-arrestin-biased CCKBR agonist that blocks CCKBR-dependent long-term potentiation.Nature communications · 2025Article
- Arrestin-biased allosteric modulator of neurotensin receptor 1 alleviates acute and chronic pain.Cell · 2025Article
- Mapping the publication trends of synaptic plasticity in neuropathic pain: A bibliometric analysis.Journal of anesthesia and translational medicine · 2024Article
- Gene therapy for chronic pain management.Cell reports. Medicine · 2024Review
- Sustained morphine exposure alters spinal NMDA receptor and astrocyte expression and exacerbates chronic pain behavior in female rats.Pain reports · 2024Article
- The multifaceted functions of β-arrestins and their therapeutic potential in neurodegenerative diseases.Experimental & molecular medicine · 2024Review
- Netrin-3 Suppresses Diabetic Neuropathic Pain by Gating the Intra-epidermal Sprouting of Sensory Axons.Neuroscience bulletin · 2023Article
- Rubbing Salt in the Wound: Molecular Evolutionary Analysis of Pain-Related Genes Reveals the Pain Adaptation of Cetaceans in Seawater.Animals : an open access journal from MDPI · 2022Article
- Hevin/Sparcl1 drives pathological pain through spinal cord astrocyte and NMDA receptor signaling.JCI insight · 2022Article
- The Involvement of Caspases in Neuroinflammation and Neuronal Apoptosis in Chronic Pain and Potential Therapeutic Targets.Frontiers in pharmacology · 2022Review
- Protective effects of miR-155-5p silencing on IFN-γ-induced apoptosis and inflammation in salivary gland epithelial cells.Experimental and therapeutic medicine · 2021Article
- Dorsal root ganglia NR2B-mediated Epac1-Piezo2 signaling pathway contributes to mechanical allodynia of bone cancer pain.Oncology letters · 2021Article
- The related mechanism of complete Freund's adjuvant-induced chronic inflammation pain based on metabolomics analysis.Biomedical chromatography : BMC · 2021Article
- Elevated Expression and Activity of Sodium Leak Channel Contributes to Neuronal Sensitization of Inflammatory Pain in Rats.Frontiers in molecular neuroscience · 2021Article
- Lysophospholipids Contribute to Oxaliplatin-Induced Acute Peripheral Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Dendritic cells in tumor microenvironment promoted the neuropathic pain via paracrine inflammatory and growth factors.Bioengineered · 2020Article
- CCL2 facilitates spinal synaptic transmission and pain via interaction with presynaptic CCR2 in spinal nociceptor terminals.Molecular brain · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Mechanisms of acute pain transition to chronic pain are not fully understood. Here we demonstrate an active role of β-arrestin 2 (Arrb2) in regulating spinal cord NMDA receptor (NMDAR) function and the duration of pain. Intrathecal injection of the mu-opioid receptor agonist [D-Ala(2), NMe-Phe(4), Gly-ol(5)]-enkephalin produces paradoxical behavioural responses: early-phase analgesia and late-phase mechanical allodynia which requires NMDAR; both phases are prolonged in Arrb2 knockout (KO) mice. Spinal administration of NMDA induces GluN2B-dependent mechanical allodynia, which is prolonged in Arrb2-KO mice and conditional KO mice lacking Arrb2 in presynaptic terminals expressing Nav1.8. Loss of Arrb2 also results in prolongation of inflammatory pain and neuropathic pain and enhancement of GluN2B-mediated NMDA currents in spinal lamina IIo not lamina I neurons. Finally, spinal over-expression of Arrb2 reverses chronic neuropathic pain after nerve injury. Thus, spinal Arrb2 may serve as an intracellular gate for acute to chronic pain transition via desensitization of NMDAR.
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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.