ArticleAnesthesiology2014
Cannabinoid receptor type 1 antagonist, AM251, attenuates mechanical allodynia and thermal hyperalgesia after burn injury.
Article in Anesthesiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 41 citations in OpenAlex.
- Cannabinoid CB1 Receptor Regulates Spinal Dorsal Horn Synaptic Plasticity in a Mouse Model of Neuropathic Pain through the CB1R/SREBP1/NAMPT/SIRT1 Metabolic Regulatory Framework.Brain and behavior · 2026Article
- Role of Concentration in Opposing Effects of Anandamide on Nociceptive Synapses versus Non-nociceptive Synapses.eNeuro · 2026Article
- Focal Adhesion Kinase Inhibition Ameliorates Burn Injury-Induced Chronic Pain in Rats.Molecular neurobiology · 2025Article
- THC Vapor Inhalation Attenuates Hyperalgesia in Rats Using a Chronic Inflammatory Pain Model.The journal of pain · 2024Article
- Characterization of a Fatty Acid Amide Hydrolase (FAAH) in Hirudo Verbana.Neurochemical research · 2024Article
- MAGL blockade alleviates steroid-induced femoral head osteonecrosis by reprogramming BMSC fate in rat.Cellular and molecular life sciences : CMLS · 2024Article
- Negative allosteric modulation of CBNeuropharmacology · 2024Article
- Protein Kinase C (PKC)-mediated TGF-β Regulation in Diabetic Neuropathy: Emphasis on Neuro-inflammation and Allodynia.Endocrine, metabolic & immune disorders drug targets · 2024Review
- A type II cannabis extract and a 1:1 blend of Δ(9)-tetrahydrocannabinol and cannabidiol display distinct antinociceptive profiles and engage different endocannabinoid targets when administered into the subarachnoid space.Frontiers in pharmacology · 2023Article
- The nonopioid cholinergic agonist GTS-21 mitigates morphine-induced aggravation of burn injury pain together with inhibition of spinal microglia activation in young rats.British journal of anaesthesia · 2022Article
- Peripherally administered cannabinoid receptor 2 (CBBrain research · 2022Article
- The Endocannabinoid System: A Potential Target for the Treatment of Various Diseases.International journal of molecular sciences · 2021Review
- Comparative studies of endocannabinoid modulation of pain.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Opioid Tolerance in Critical Illness.The New England journal of medicine · 2019Review
- Insights From Molecular Dynamics Simulations of a Number of G-Protein Coupled Receptor Targets for the Treatment of Pain and Opioid Use Disorders.Frontiers in molecular neuroscience · 2019Review
- Cannabinoid 1 receptor knockout mice display cold allodynia, but enhanced recovery from spared-nerve injury-induced mechanical hypersensitivity.Molecular pain · 2016Article
- A pro-nociceptive phenotype unmasked in mice lacking fatty-acid amide hydrolase.Molecular pain · 2016Article
- Acute and perioperative care of the burn-injured patient.Anesthesiology · 2015Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundBurn injury causes nociceptive behaviors, and inflammation-related pathologic pain can lead to glial cell activation. This study tested the hypothesis that burn injury activates glial cells, and cannabinoid receptor 1 (CB1R) antagonist, AM251, will decrease burn pain.
methodsAnesthetized rats received 0.75-cm third-degree burn on dorsal hind paw. Vehicle or AM251 30 μg intrathecally (older rats, n=6 per group) or, either vehicle, 0.1 or 1.0 mg/kg intraperitoneally (younger rats, n=6 per group), started immediate postburn, was administered for 7 days. Mechanical allodynia and thermal hyperalgesia were tested on ventral paw for 14 days. Microglial and astroglial activity was assessed by immunocytochemistry.
resultsAllodynia, observed on burn side from day 1 to 14, was significantly (P<0.05) attenuated by intrathecal and intraperitoneal AM251 (1 mg/kg) starting from 3 to 14 days. Hyperalgesia, observed from day 3 to 12, was completely (P<0.05) reversed by intrathecal and intraperitoneal AM251 (1 mg/kg). AM251 0.1 mg/kg had no effect. Microglial activity (n=3 per time point) increased (P<0.05) 18.5±7.5 and 12.3±1.6 (mean±SD) fold at 7 and 14 days, respectively. Astroglial activity (n=4 per time point) increased 2.9±0.3 fold at day 7 only. Glial activities were unaltered by AM251.
conclusionsAM251 inhibited nociceptive behaviors after burn even beyond 7-day period of administration. Although many studies have documented the utility of CB1R agonists, this study indicates that endogenous cannabinoids may have an unexpected pronociceptive effect during development of burn pain, explaining why CB1R antagonist, AM251, improves nociceptive behaviors. The decreased nociception with AM251 without altering glial activity indicates that AM251 acts further downstream of activated glial cells.
Indexed as
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.