N-arachidonoyl glycine,an abundant endogenous lipid,potently drives directed cellular migration through GPR18, the putative abnormal cannabidiol receptor |
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| Authors: | Douglas McHugh Sherry SJ Hu Neta Rimmerman Ana Juknat Zvi Vogel J Michael Walker Heather B Bradshaw |
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| Affiliation: | (1) The Department of Psychological and Brain Sciences, Indiana University, 1101 East 10th Street, 47405 Bloomington, IN, USA;(2) The Gill Center for Biomolecular Science, Indiana University, 1101 East 10th Street, 47405 Bloomington, IN, USA;(3) The Neurobiology Department, Weizmann Institute of Science, Rehovot, Israel;(4) The Adelson Center for the Biology of Addictive Diseases, Sackler Faculty of Medicine, Tel Aviv University, Israel |
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| Abstract: | Background Microglia provide continuous immune surveillance of the CNS and upon activation rapidly change phenotype to express receptors that respond to chemoattractants during CNS damage or infection. These activated microglia undergo directed migration towards affected tissue. Importantly, the molecular species of chemoattractant encountered determines if microglia respond with pro- or anti-inflammatory behaviour, yet the signaling molecules that trigger migration remain poorly understood. The endogenous cannabinoid system regulates microglial migration via CB2 receptors and an as yet unidentified GPCR termed the 'abnormal cannabidiol' (Abn-CBD) receptor. Abn-CBD is a synthetic isomer of the phytocannabinoid cannabidiol (CBD) and is inactive at CB1 or CB2 receptors, but functions as a selective agonist at this Gi/o-coupled GPCR. N-arachidonoyl glycine (NAGly) is an endogenous metabolite of the endocannabinoid anandamide and acts as an efficacious agonist at GPR18. Here, we investigate the relationship between NAGly, Abn-CBD, the unidentified 'Abn-CBD' receptor, GPR18, and BV-2 microglial migration. |
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