ArticleISRN anesthesiology2011
The Central Role of Glia in Pathological Pain and the Potential of Targeting the Cannabinoid 2 Receptor for Pain Relief.
Article in ISRN anesthesiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
11 citing papers in PubMed, 21 citations in OpenAlex.
- Antinociceptive effects of intrathecal neuropeptide B/W receptor 1 agonists in mouse acute nociception, peripheral neuropathy, and inflammatory pain models.Pharmacological reports : PR · 2025Article
- Article
- Satellite Glial Cells in Pain Research: A Targeted Viewpoint of Potential and Future Directions.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Aging-Related Phenotypic Conversion of Medullary Microglia Enhances Intraoral Incisional Pain Sensitivity.International journal of molecular sciences · 2020Article
- CCR4 Antagonist (C021) Administration Diminishes Hypersensitivity and Enhances the Analgesic Potency of Morphine and Buprenorphine in a Mouse Model of Neuropathic Pain.Frontiers in immunology · 2020Article
- The Effects of Morphine, Baclofen, and Buspirone Alone and in Combination on Schedule-Controlled Responding and Hot Plate Antinociception in Rats.The Journal of pharmacology and experimental therapeutics · 2019Article
- Cytokines in Pain: Harnessing Endogenous Anti-Inflammatory Signaling for Improved Pain Management.Frontiers in immunology · 2019Review
- Systemic Lipopolysaccharide-Induced Pain Sensitivity and Spinal Inflammation Were Reduced by Minocycline in Neonatal Rats.International journal of molecular sciences · 2018Article
- Synergistic attenuation of chronic pain using mu opioid and cannabinoid receptor 2 agonists.Neuropharmacology · 2017Article
- Palmitoylethanolamide, a naturally occurring disease-modifying agent in neuropathic pain.Inflammopharmacology · 2014Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Under normal conditions, acute pain processing consists of well-characterized neuronal signaling events. When dysfunctional pain signaling occurs, pathological pain ensues. Glial activation and their released factors participate in the mediation of pathological pain. The use of cannabinoid compounds for pain relief is currently an area of great interest for both basic scientists and physicians. These compounds, bind mainly either the cannabinoid receptor subtype 1 (CB(1)R) or cannabinoid receptor subtype 2 (CB(2)R) and are able to modulate pain. Although cannabinoids were initially only thought to modulate pain via neuronal mechanisms within the central nervous system, strong evidence now supports that CB(2)R cannabinoid compounds are capable of modulating glia, (e.g. astrocytes and microglia) for pain relief. However, the mechanisms underlying cannabinoid receptor-mediated pain relief remain largely unknown. An emerging body of evidence supports that CB(2)R agonist compounds may prove to be powerful novel therapeutic candidates for the treatment of chronic pain.
Identifiers
What OpenQuestion holds
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.