ArticleBritish journal of pharmacology2020
Inhibition of fatty acid amide hydrolase in the CNS prevents and reverses morphine tolerance in male and female mice.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
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- NAAA-regulated lipid signaling in monocytes controls the induction of hyperalgesic priming in mice.Nature communications · 2024Article
- A Sensitive Ultrahigh-Performance Liquid Chromatography/Tandem Mass Spectrometry Method for the Simultaneous Analysis of Phytocannabinoids and Endocannabinoids in Plasma and Brain.Cannabis and cannabinoid research · 2024Article
- Targeting NAAA counters dopamine neuron loss and symptom progression in mouse models of parkinsonism.Pharmacological research · 2022Article
- (Wh)olistic (E)ndocannabinoidome-Microbiome-Axis Modulation through (N)utrition (WHEN) to Curb Obesity and Related Disorders.Lipids in health and disease · 2022Review
- Persistent Exposure to ΔThe Journal of pharmacology and experimental therapeutics · 2021Article
- Relevance of Peroxisome Proliferator Activated Receptors in Multitarget Paradigm Associated with the Endocannabinoid System.International journal of molecular sciences · 2021Review
- PMSF Attenuates Morphine Antinociceptive Tolerance and Dependence in Mice: Its Association with the Oxidative Stress Suppression.Iranian journal of pharmaceutical research : IJPR · 2021Article
- Article
- Inhibition of fatty acid amide hydrolase in the CNS prevents and reverses morphine tolerance in male and female mice.British journal of pharmacology · 2020Article
- Positive Allosteric Modulation of CBFrontiers in molecular neuroscience · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeFatty acid amide hydrolase (FAAH) is an intracellular serine amidase that terminates the signalling of various lipid messengers involved in pain regulation, including anandamide and palmitoylethanolamide. Here, we investigated the effects of pharmacological or genetic FAAH removal on tolerance to the anti-nociceptive effects of morphine. EXPERIMENTAL APPROACH: We induced tolerance in male and female mice by administering twice-daily morphine for 7 days while monitoring nociceptive thresholds by the tail immersion test. The globally active FAAH inhibitor URB597 (1 and 3 mg·kg KEY
resultsURB597 prevented and reversed morphine tolerance in both male and female mice. This effect was mimicked by genetic FAAH deletion, but not by URB937. Treatment with AM630 suppressed, whereas treatment with AM251 or GW6471, attenuated the effects of URB597. Anandamide mobilization was enhanced in the spinal cord of morphine-tolerant mice. mRNA levels of the anandamide-producing enzyme N-acyl-phosphatidylethanolamine PLD (NAPE-PLD) and the palmitoylethanolamide receptor PPAR-α, but not those for CB
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