The non-psychotropic cannabinoid (+)-(3S,4S)-7-hydroxy-Δ6-tetrahydrocannabinol 1,1-dimethylheptyl (HU-211) attenuates receptor-mediated neurotoxicity in primary cultures of rat forebrain
References (21)
Glutamate neurotoxicity and diseases of the nervous system
Neuron
(1988)- et al.
Amino acid neurotoxicity: intracellular sites of calcium accumulation associated with the onset of irreversible damage to rat cerebellar neurons in vitro
Neurosci. Lett.
(1986) - et al.
Stereochemical effects of 11-OH-delta8-tetrahydrocannabinol-dimethylheptyl to inhibit adenylate cyclase and to bind the cannabinoid receptor
Neuropharmacology
(1990) - et al.
Quantitative determination of glutamate mediated cortical neuronal injury in cell culture by lactate dehydrogenase efflux assay
J. Neurosci. Methods
(1987) - et al.
Stereochemical effects of M-OH-delta-8-THC-dimethylheptyl in mice and dogs
Pharmacol. Biochem. Behav.
(1989) - et al.
Syntheśis of the individual, pharmacology distinct, enantiomers of a tetrahydrocannabinol derivative
Tetrahedron Asymmetry
(1990) - et al.
Metabotropic glutamate receptors in brain function and pathology
Trends Pharmacol. Sci.
(1993) - et al.
Structureactivity relationships in the development of excitatory amino acid receptor agonists and competitive antagonists
Trends Pharmacol. Sci.
(1990) - et al.
Quisqualate and kainate-activated channels in mouse central neurons in culture
J. Physiol.
(1988) Metabolic imbalance and nerve cell damage in the brain
Prog. Brain Res.
(1988)
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2018, Biochemical PharmacologyCitation Excerpt :CB2 receptor agonists exhibit inhibitory effects on butyrylcholinesterase [90]. The synthetic cannabinoid HU-211 inhibits NMDA receptors, thereby protecting cells from glutamate-induced neurotoxicity [91–93]. CB1 receptors mediate neuroprotection against excitotoxicity by inhibiting presynaptic glutamate release [94] and excessive calcium release [95–97].
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2010, Journal of Biological ChemistryCitation Excerpt :However, in this experiment, higher concentrations (>2 μm for 2-AG and >10 μm for AEA) induced a significant increase in DNA fragmentation compared with control cells, thus representing the neuroprotection/neurotoxicity paradox of endocannabinoid modulation, which has been the focus of a recent review (45). Consistent with our finding, other studies have reported on the neuroprotective properties of the endocannabinoid system in hippocampal and cortical neurons against a number of toxic insults, including excitotoxicity (22, 46), ischemia (47), and oxidative damage (23), all of which are known to induce cell death by apoptosis. This endocannabinoid-mediated neuroprotection has been reported to occur through a variety of mechanisms, including activation of prosurvival signaling pathways like inositol triphosphate (48), PI3K (49), focal adhesion kinase (50), and ERK (49–50) as well as through inhibition of calcium currents and opening of potassium channels (51–53).
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