Abstract
Exogenous cannabinoids, such as delta9-tetrahydrocannabinol (THC), as well as the modulation of endogenous cannabinoids, affect cognitive function through the activation of cannabinoid receptors. Indeed, these compounds modulate a number of signalling pathways critically implicated in the deleterious effect of cannabinoids on learning and memory. Thus, the involvement of the mammalian target of rapamycin pathway and extracellular signal-regulated kinases, together with their consequent regulation of cellular processes such as protein translation, play a critical role in the amnesic-like effects of cannabinoids. In this study, we summarize the cellular and molecular mechanisms reported in the modulation of cognitive function by the endocannabinoid system.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Arachidonic Acids / antagonists & inhibitors
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Arachidonic Acids / metabolism
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Cannabinoid Receptor Agonists / metabolism
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Cannabinoid Receptor Agonists / pharmacology
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Cognition / drug effects
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Cognition Disorders / chemically induced*
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Cognition Disorders / metabolism
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Dronabinol / adverse effects*
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Endocannabinoids / antagonists & inhibitors
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Endocannabinoids / metabolism
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Glycerides / antagonists & inhibitors
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Glycerides / metabolism
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Hippocampus / metabolism
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Hippocampus / physiopathology
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Humans
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Memory / drug effects
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Neuronal Plasticity
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Polyunsaturated Alkamides / antagonists & inhibitors
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Polyunsaturated Alkamides / metabolism
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Receptor, Cannabinoid, CB1 / metabolism*
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Synaptic Transmission
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TOR Serine-Threonine Kinases / metabolism
Substances
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Arachidonic Acids
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Cannabinoid Receptor Agonists
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Endocannabinoids
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Glycerides
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Polyunsaturated Alkamides
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Receptor, Cannabinoid, CB1
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Dronabinol
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glyceryl 2-arachidonate
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MTOR protein, human
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TOR Serine-Threonine Kinases
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anandamide