The objective of this study was to investigate whether single and repeated administration of the cannabinoids anandamide or Delta(9)-tetrahydrocannabinol affected brain energetic metabolism. Single administration of either anandamide (20 mg/kg) or Delta(9)-tetrahydrocannabinol (10 mg/kg) in rats induced a behaviour typical with cannabinoids. An increase in both brain mitochondria oxidative phosphorylation and cerebral lipoperoxidation was shown ex vivo. The cannabinoid CB1 receptor-specific antagonist, N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide (SR141716A; 3 mg/kg), reversed the anandamide-induced metabolic effects. Prolonged exposure to anandamide (20 mg/kg, 16 days) induced behavioural tolerance and the disappearance of the increased mitochondria oxygen uptake and lipoperoxidation. Repeated Delta(9)-tetrahydrocannabinol injection (10 mg/kg, twice daily, 4.5 days) reduced brain metabolism and uncoupled respiration from oxidative phosphorylation. The present findings showed that both anandamide and Delta(9)-tetrahydrocannabinol enhanced the energetic brain metabolism, probably via the cannabinoid CB1 receptor; the anandamide-tolerant brain of rats showed tolerance to the drug for metabolic effects, while the brain of Delta(9)-tetrahydrocannabinol-tolerant rats showed metabolic signs of neuronal damage, i.e. low energy production

Costa, B., Colleoni, M. (2000). Changes in rat brain energetic metabolism after exposure to anandamide or Delta(9)-tetrahydrocannabinol. EUROPEAN JOURNAL OF PHARMACOLOGY, 395(1), 1-7 [10.1016/S0014-2999(00)00170-9].

Changes in rat brain energetic metabolism after exposure to anandamide or Delta(9)-tetrahydrocannabinol

Costa, BS;
2000

Abstract

The objective of this study was to investigate whether single and repeated administration of the cannabinoids anandamide or Delta(9)-tetrahydrocannabinol affected brain energetic metabolism. Single administration of either anandamide (20 mg/kg) or Delta(9)-tetrahydrocannabinol (10 mg/kg) in rats induced a behaviour typical with cannabinoids. An increase in both brain mitochondria oxidative phosphorylation and cerebral lipoperoxidation was shown ex vivo. The cannabinoid CB1 receptor-specific antagonist, N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide (SR141716A; 3 mg/kg), reversed the anandamide-induced metabolic effects. Prolonged exposure to anandamide (20 mg/kg, 16 days) induced behavioural tolerance and the disappearance of the increased mitochondria oxygen uptake and lipoperoxidation. Repeated Delta(9)-tetrahydrocannabinol injection (10 mg/kg, twice daily, 4.5 days) reduced brain metabolism and uncoupled respiration from oxidative phosphorylation. The present findings showed that both anandamide and Delta(9)-tetrahydrocannabinol enhanced the energetic brain metabolism, probably via the cannabinoid CB1 receptor; the anandamide-tolerant brain of rats showed tolerance to the drug for metabolic effects, while the brain of Delta(9)-tetrahydrocannabinol-tolerant rats showed metabolic signs of neuronal damage, i.e. low energy production
Articolo in rivista - Articolo scientifico
cannabinoid; behavioural tolerance; brain; energetic metabolism; cannabinoid cb1 receptor-specific antagonist
English
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Costa, B., Colleoni, M. (2000). Changes in rat brain energetic metabolism after exposure to anandamide or Delta(9)-tetrahydrocannabinol. EUROPEAN JOURNAL OF PHARMACOLOGY, 395(1), 1-7 [10.1016/S0014-2999(00)00170-9].
Costa, B; Colleoni, M
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/4154
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