ArticleInternational journal of molecular sciences2019
Protective Effect of N-Arachidonoyl Glycine-GPR18 Signaling after Excitotoxical Lesion in Murine Organotypic Hippocampal Slice Cultures.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Cannabinoid receptor type 1 deficiency protects from lipopolysaccharide-induced preterm birth: the role of the decidual endocannabinoid system.Reproduction (Cambridge, England) · 2026Article
- Orphan GPCRs in Neurodegenerative Disorders: Integrating Structural Biology and Drug Discovery Approaches.Current issues in molecular biology · 2024Review
- N-arachidonylglycine is a caloric state-dependent circulating metabolite which regulates human CD4iScience · 2023Article
- Deciphering Complex Interactions in Bioactive Lipid Signaling.Molecules (Basel, Switzerland) · 2023Article
- Endocannabinoid signaling in astrocytes.Glia · 2023Review
- Nimodipine Exerts Time-Dependent Neuroprotective Effect after Excitotoxical Damage in Organotypic Slice Cultures.International journal of molecular sciences · 2022Article
- Article
- Interaction of Glia Cells with Glioblastoma and Melanoma Cells under the Influence of Phytocannabinoids.Cells · 2022Article
- Microglia-Dependent and Independent Brain Cytoprotective Effects of Mycophenolate Mofetil During Neuronal Damage.Frontiers in aging neuroscience · 2022Article
- Receptor-Dependent and Independent Regulation of Voltage-Gated CaInternational journal of molecular sciences · 2021Review
- GPR18 drives FAAH inhibition-induced neuroprotection against HIV-1 Tat-induced neurodegeneration.Experimental neurology · 2021Article
- THC Reduces Ki67-Immunoreactive Cells Derived from Human Primary Glioblastoma in a GPR55-Dependent Manner.Cancers · 2021Article
- Assessment of Neuronal Damage in Brain Slice Cultures Using Machine Learning Based on Spatial Features.Frontiers in neuroscience · 2021Article
- Specialized Pro-resolving Lipid Mediators and Glial Cells: Emerging Candidates for Brain Homeostasis and Repair.Frontiers in cellular neuroscience · 2021Review
- Therapeutic Exploitation of GPR18: Beyond the Cannabinoids?Journal of medicinal chemistry · 2020Review
- Resolvin D1 and D2 inhibit tumour growth and inflammation via modulating macrophage polarization.Journal of cellular and molecular medicine · 2020Article
- Organotypic Brain Slice Culture Microglia Exhibit Molecular Similarity to Acutely-Isolated Adult Microglia and Provide a Platform to Study Neuroinflammation.Frontiers in cellular neuroscience · 2020Article
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
N-arachidonoyl glycine (NAGly) is an endocannabinoid involved in the regulation of different immune cells. It was shown to activate the GPR18 receptor, which was postulated to switch macrophages from cytotoxic to reparative. To study GPR18 expression and neuroprotection after NAGly treatment we used excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). The effect of NAGly was also tested in isolated microglia and astrocytes as these cells play a crucial role during neuronal injury. In the present study, the GPR18 receptor was found in OHSC at mRNA level and was downregulated after N-Methyl-D-aspartate (NMDA) treatment at a single time point. Furthermore, treatment with NAGly reduced neuronal damage and this effect was abolished by GPR18 and cannabinoid receptor (CB)₂ receptor antagonists. The activation but not motility of primary microglia and astrocytes was influenced when incubated with NAGly. However, NAGly alone reduced the phosphorylation of Akt but no changes in activation of the p44/42 and p38 MAPK and CREB pathways in BV2 cells could be observed. Given NAGly mediated actions we speculate that GPR18 and its ligand NAGly are modulators of glial and neuronal cells during neuronal damage.
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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.