A Cannabinoid Receptor-Mediated Mechanism Participates in the Neuroprotective Effects of Oleamide Against Excitotoxic Damage in Rat Brain Synaptosomes and Cortical Slices

Cannabinoid-profiled agents improve cell survival via reduction of oxidative stress and inflammation, and Nrf2 activation in a toxic model combining hyperglycemia+Aβ1-42 peptide in rat hippocampal neurons

“…The levels of protection displayed by these agents for different toxic endpoints suggest their broad spectrum of neuromodulatory actions at different cell levels. Neuroprotective effects of endocannabinoids, synthetic cannabinoids, and the inhibitor of FAAH, URB597, have been recently reported in other toxic models combining excitotoxicity and oxidative damage (Rangel-López et al, 2015;Aguilera-Portillo et al, 2019;Maya-López et al, 2019;Kotlar et al, 2019).…”

“…FAAH is widely localized throughout the brain, and FAAH-positive neurons have been found in the proximity of nerve terminals containing CB1 in the neocortex, hippocampus and basal ganglia (De Petrocellis et al, 2004). The pharmacological tool [3-(3carbamoylphenyl)phenyl]N-cyclohexylcarbamate (URB597) exhibits unique therapeutic potential as it is capable of inhibiting FAAH activity, thereby leading to accumulation of endocannabinoids, such as AEA and oleamide (Aguilera-Portillo et al, 2019;Maya-López et al, 2019). 2-Arachidonoylglycerol (2-AG), another major endocannabinoid which is mainly degraded by monoacylglycerol lipase (MAGL), has been shown to activate CB1 and CB2 receptors, in turn, exerting neuroprotective effects (Dinh et al, 2002;Mounsey et al, 2015).…”

Comparing the Neuroprotective Effects of Caffeic Acid in Rat Cortical Slices and Caenorhabditis elegans: Involvement of Nrf2 and SKN-1 Signaling Pathways

“…Assessment of cell damage in cortical slices-To visually define cells undergoing damage, a method based on immunofluorescence was used, according to a previous report (Maya-López et al 2019). Cortical slices already exposed to the different experimental conditions were loaded with propidium iodide (PI, 100 μg/ml, Roche) for 10 min.…”

Mild Traumatic Brain Injury Contributes to the Development of Delayed Neuroinflammation

“…Microglial cells undergo a process of differentiation and activation after injury, and at these stages, the expression pattern of the CB1R and CB2R also changes [23]. Cannabinoid receptor agonists have been shown to inhibit mitochondrial dysfunction associated with excitotoxic brain damage [40] and suppress the production of pro-inflammatory cytokines [41]. The data obtained in this study indicate an increase in the synthesis of CB1R in the cerebral cortex of rats on the 7th day after mTBI.…”