ReviewMolecular brain2011
Neuronal and microglial mechanisms of neuropathic pain.
Review in Molecular brain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
116 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Platelet-Rich Plasma Modulates Neuroinflammation in an iPSC Model of Sensory Neurons and Microglia.International journal of molecular sciences · 2026Article
- S1P receptor 1 antagonist ponesimod alleviates postherpetic neuralgia in rats by normalizing spinal TRPV1 expression and inhibiting MAPK-mediated glial activation.Cytotechnology · 2025Article
- Sensory neuron-specific block of multifaceted sodium channels mitigates neuropathic pain behaviors of osteoarthritis.Pain reports · 2025Article
- Optogenetic activation of cortical microglia promotes neuronal activity and pain hypersensitivity.Cell reports · 2025Article
- Chemogenetic activation of microglial Gi signaling decreases microglial surveillance and impairs neuronal synchronization.Science advances · 2025Article
- The Golden Year? Early Intervention Yields Superior Outcomes in Chronic Pelvic Pain with Pudendal Neuralgia: A Comparative Analysis of Early vs. Delayed Treatment.Life (Basel, Switzerland) · 2025Article
- Identification of potential drug-induced neuralgia signals through disproportionality analysis of the FAERS database.Frontiers in pharmacology · 2025Article
- The influence of sex on neuroimmune communication, pain, and physiology.Biology of sex differences · 2024Review
- A Single Injection of rAAV-shmTOR in Peripheral Nerve Persistently Attenuates Nerve Injury-Induced Mechanical Allodynia.International journal of molecular sciences · 2023Article
- Cathepsin S Upregulation Measured in the Peripheral Blood Mononuclear Cells Prior to Surgery Points to Postoperative Pain Development in Patients with Hip Osteoarthritis.Diagnostics (Basel, Switzerland) · 2023Article
- Chemogenetic and Optogenetic Manipulations of Microglia in Chronic Pain.Neuroscience bulletin · 2023Review
- Green Light Exposure Elicits Anti-inflammation, Endogenous Opioid Release and Dampens Synaptic Potentiation to Relieve Post-surgical Pain.The journal of pain · 2023Article
- Neuronal CRMP2 phosphorylation inhibition by the flavonoid, naringenin, contributes to the reversal of spinal sensitization and arthritic pain improvement.Arthritis research & therapy · 2022Article
- Exploring pharmacological inhibition of GBritish journal of pharmacology · 2022Article
- Utilizing multiphoton imaging and integrative clearing to reveal sex differences in neuroimmune interactions after nerve injury.Neural regeneration research · 2022Article
- Spinal microglia contribute to sustained inflammatory pain via amplifying neuronal activity.Molecular brain · 2022Article
- The efficacy of minocycline hydrochloride ointment versus iodoform gauze for alveolar osteitis: A prospective cohort study.BMC oral health · 2022Article
- NFAT1 Orchestrates Spinal Microglial Transcription and Promotes Microglial Proliferation via c-MYC Contributing to Nerve Injury-Induced Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Selective block of sensory neuronal T-type/Cav3.2 activity mitigates neuropathic pain behavior in a rat model of osteoarthritis pain.Arthritis research & therapy · 2022Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Neuropathic pain is generally defined as a chronic pain state resulting from peripheral and/or central nerve injury. Effective treatment for neuropathic pain is still lacking, due in part to poor understanding of pathological mechanisms at the molecular level. Neuronal mechanisms of neuropathic pain, especially synaptic plasticity, are the major focus of many investigators. N-methyl-D-aspartate (NMDA) receptor dependent synaptic plasticity at the spinal and cortical levels is believed to contribute to enhanced sensory responses after injury. Glial cells, including astrocytes and microglia, have recently been implicated in neuropathic pain. These glial cells form close interactions with neurons and thus may modulate nociceptive transmission under pathological conditions. In this review, we present recent progress in the study of neuronal and microglial mechanisms underlying neuropathic pain. We propose that activity-dependent neuronal plasticity is a key target for treatment in neuropathic 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.