FEBS Letters · 1998 · 284 citations · 22 references
Life SciencesNeurosciencePharmacologyApoptosisNeurochemistryNeuropharmacologyApoptosis PharmacologyApoptosis RegulationApoptotic SignalingCannabinoid PharmacologyCell DeathNeuronal Cell DeathAntagonist ActivityCannabinoid Receptor ModulationCannabinoid Receptor PharmacologyCeramide MetabolismMembrane Phospholipid AsymmetryPlasma Membrane AsymmetrySphingomyelin BiosynthesisSphingomyelin Metabolism
delta9-Tetrahydrocannabinol (THC), the major active component of marijuana, induced apoptosis in C6.9 glioma cells, as determined by DNA fragmentation and loss of plasma membrane asymmetry. THC stimulated sphingomyelin hydrolysis in C6.9 glioma cells. THC and N-acetylsphingosine, a cell-permeable ceramide analog, induced apoptosis in several transformed neural cells but not in primary astrocytes or neurons. Although glioma C6.9 cells expressed the CBI cannabinoid receptor, neither THC-induced apoptosis nor THC-induced sphingomyelin breakdown were prevented by SR141716, a specific antagonist of that receptor. Results thus show that THC-induced apoptosis in glioma C6.9 cells may rely on a CBI receptor-independent stimulation of sphingomyelin breakdown.
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Isolation and Structure of a Brain Constituent That Binds to the Cannabinoid Receptor
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Molecular characterization of a peripheral receptor for cannabinoids
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SR141716A, a potent and selective antagonist of the brain cannabinoid receptor
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Medicine, Neuroscience, Pharmacology +14