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Open AccessArticle

CB2 Receptors and Neuron–Glia Interactions Modulate Neurotoxicity Generated by MAGL Inhibition

1
Facultad de Ciencias, Departamento de Bioquímica y Genética, Universidad de Navarra, 31008 Pamplona, Spain
2
CIMA, Programa de Neurociencias, Universidad de Navarra, 31008 Pamplona, Spain
3
Facultad de Medicina, Departamento de Patología, Anatomía y Fisiología, Universidad de Navarra, 31008 Pamplona, Spain
4
IdiSNA, Instituto de Investigación Sanitaria de Navarra, 31008 Pamplona, Spain
*
Author to whom correspondence should be addressed.
Present address: Facultad de Ciencias de la Salud, Programa de Medicina, Universidad de Manizales, Cra 9a ### 1903, 170001 Manizales, Colombia.
These two authors contributed equally to this work.
§
Senior authors of this study.
Biomolecules 2020, 10(8), 1198; https://doi.org/10.3390/biom10081198
Received: 30 June 2020 / Revised: 30 July 2020 / Accepted: 12 August 2020 / Published: 18 August 2020
(This article belongs to the Special Issue The Endocannabinoid System in Health and Disease)
Monoacylglycerol lipase inhibition (MAGL) has emerged as an interesting therapeutic target for neurodegenerative disease treatment due to its ability to modulate the endocannabinoid system and to prevent the production of proinflammatory mediators. To obtain a beneficial response, it is necessary to understand how this inhibition affects the neuron–glia crosstalk and neuron viability. In this study, the effect of MAGL inhibition by KML29 was evaluated in two types of rat cortical primary cultures; mixed cultures, including neuron and glial cells, and neuron-enriched cultures. The risk of neuronal death was estimated by longitudinal survival analysis. The spontaneous neuronal risk of death in culture was higher in the absence of glial cells, a process that was enhanced by KML29 addition. In contrast, neuronal survival was not compromised by MAGL inhibition in the presence of glial cells. Blockade of cannabinoid type 2 (CB2) receptors expressed mainly by microglial cells did not affect the spontaneous neuronal death risk but decreased neuronal survival when KML29 was added. Modulation of cannabinoid type 1 (CB1) receptors did not affect neuronal survival. Our results show that neuron–glia interactions are essential for neuronal survival. CB2 receptors play a key role in these protective interactions when neurons are exposed to toxic conditions. View Full-Text
Keywords: monoacylglycerol lipase; endocannabinoid system; CB2 receptors; microglia; neuroprotection; KML29 monoacylglycerol lipase; endocannabinoid system; CB2 receptors; microglia; neuroprotection; KML29
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MDPI and ACS Style

Rojo-Bustamante, E.; Íñigo-Marco, I.; Abellanas, M.A.; Vinueza-Gavilanes, R.; Baltanás, A.; Luquin, E.; Arrasate, M.; Aymerich, M.S. CB2 Receptors and Neuron–Glia Interactions Modulate Neurotoxicity Generated by MAGL Inhibition. Biomolecules 2020, 10, 1198. https://doi.org/10.3390/biom10081198

AMA Style

Rojo-Bustamante E, Íñigo-Marco I, Abellanas MA, Vinueza-Gavilanes R, Baltanás A, Luquin E, Arrasate M, Aymerich MS. CB2 Receptors and Neuron–Glia Interactions Modulate Neurotoxicity Generated by MAGL Inhibition. Biomolecules. 2020; 10(8):1198. https://doi.org/10.3390/biom10081198

Chicago/Turabian Style

Rojo-Bustamante, Estefania; Íñigo-Marco, Ignacio; Abellanas, Miguel A.; Vinueza-Gavilanes, Rodrigo; Baltanás, Ana; Luquin, Esther; Arrasate, Montserrat; Aymerich, Maria S. 2020. "CB2 Receptors and Neuron–Glia Interactions Modulate Neurotoxicity Generated by MAGL Inhibition" Biomolecules 10, no. 8: 1198. https://doi.org/10.3390/biom10081198

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