ArticleThe Journal of pharmacology and experimental therapeutics2010
Cyclooxygenase-2 mediates anandamide metabolism in the mouse brain.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 44 citations in OpenAlex.
- Assessment of NSAIDs as potential inhibitors of the fatty acid amide hydrolase I (FAAH-1) using three different primary fatty acid amide substrates in vitro.BMC pharmacology & toxicology · 2022Article
- On the Biomedical Properties of Endocannabinoid Degradation and Reuptake Inhibitors: Pre-clinical and Clinical Evidence.Neurotoxicity research · 2021Review
- Contribution of T-Type Calcium Channels to Spinal Cord Injury-Induced Hyperexcitability of Nociceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Role of the endocannabinoid system in vertebrates: Emphasis on the zebrafish model.Development, growth & differentiation · 2017Review
- Article
- Substrate-selective COX-2 inhibition as a novel strategy for therapeutic endocannabinoid augmentation.Trends in pharmacological sciences · 2014Review
- Regulation of circulating endocannabinoids associated with cancer and metastases in mice and humans.Oncoscience · 2014Article
- Endocannabinoid signaling in the etiology and treatment of major depressive illness.Current pharmaceutical design · 2014Review
- Substrate-selective COX-2 inhibition decreases anxiety via endocannabinoid activation.Nature neuroscience · 2013Article
- Monoacylglycerol lipase - a target for drug development?British journal of pharmacology · 2012Review
- Fatty acid-binding proteins transport N-acylethanolamines to nuclear receptors and are targets of endocannabinoid transport inhibitors.The Journal of biological chemistry · 2012Article
- Discovery of prostamide F2α and its role in inflammatory pain and dorsal horn nociceptive neuron hyperexcitability.PloS one · 2012Article
- Peripheral effects of FAAH deficiency on fuel and energy homeostasis: role of dysregulated lysine acetylation.PloS one · 2012Article
- (R)-Profens are substrate-selective inhibitors of endocannabinoid oxygenation by COX-2.Nature chemical biology · 2011Article
- Endocannabinoid oxygenation by cyclooxygenases, lipoxygenases, and cytochromes P450: cross-talk between the eicosanoid and endocannabinoid signaling pathways.Chemical reviews · 2011Review
- The abused inhalant toluene differentially modulates excitatory and inhibitory synaptic transmission in deep-layer neurons of the medial prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- Lipoxygenase-mediated oxidation of polyunsaturated N-acylethanolamines in Arabidopsis.The Journal of biological chemistry · 2011Article
- A methodology for radiolabeling of the endocannabinoid 2-arachidonoylglycerol (2-AG).The Journal of organic chemistry · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cyclooxygenase-2 (COX-2) mediates inflammation and contributes to neurodegeneration. Best known for its pathological up-regulation, COX-2 is also constitutively expressed within the brain and mediates synaptic transmission through prostaglandin synthesis. Along with arachidonic acid, COX-2 oxygenates the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol in vitro. Inhibition of COX-2 enhances retrograde signaling in the hippocampus, suggesting COX-2 mediates endocannabinoid tone in healthy brain. The degree to which COX-2 may regulate endocannabinoid metabolism in vivo is currently unclear. Therefore, we explored the effect of COX-2 inhibition on [(3)H]AEA metabolism in mouse brain. Although AEA is hydrolyzed primarily by fatty acid amide hydrolase (FAAH), ex vivo autoradiography revealed that COX-2 inhibition by nimesulide redirected [(3)H]AEA substrate from COX-2 to FAAH in the cortex, hippocampus, thalamus, and periaqueductal gray. These data indicate that COX-2 possesses the capacity to metabolize AEA in vivo and can compete with FAAH for AEA in several brain regions. Temporal fluctuations in COX-2 expression were observed in the brain, with an increase in COX-2 protein and mRNA in the hippocampus at midnight compared with noon. COX-2 immunolocalization was robust in the hippocampus and several cortical regions. Although most regions exhibited no temporal changes in COX-2 immunolocalization, increased numbers of immunoreactive cells were detected at midnight in layers II and III of the somatosensory and visual cortices. These temporal variations in COX-2 distribution reduced the enzyme's contribution toward [(3)H]AEA metabolism in the somatosensory cortex at midnight. Taken together, our findings establish COX-2 as a mediator of regional AEA metabolism in mouse brain.
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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.