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Title: Protective effect of n-arachidonoyl glycine-GPR18 signaling after excitotoxical lesion in murine organotypic hippocampal slice cultures
Author(s): Hohmann, UrszulaLook up in the Integrated Authority File of the German National Library
Hohmann, Tim
Ghadban, Chalid
Rothgänger, Candy
Wong, Daniel
Antonietti, Alexandra
Groth, ThomasLook up in the Integrated Authority File of the German National Library
Mackie, Ken
Dehghani, Faramarz
Issue Date: 2019
Type: Article
Language: English
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.
Open Access: Open access publication
License: (CC BY 4.0) Creative Commons Attribution 4.0(CC BY 4.0) Creative Commons Attribution 4.0
Sponsor/Funder: Publikationsfond MLU
Journal Title: International journal of molecular sciences
Publisher: MDPI
Publisher Place: Basel
Volume: 20
Issue: 6
Original Publication: 10.3390/ijms20061266
Appears in Collections:Open Access Publikationen der MLU

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