For the evaluation of pharmacological effects on cognition several animal models are used that measure different aspects of cognition. These models are shortly discussed and positioned in a schematic overview of cognition that consists of a central executive function that directs the information processing between the sensory input, a long-term or reference memory store, two working memory “slave” systems (e.g. the phonological loop and the visuo-spatial sketch path) and the motor output. Subsequently, the effects of CB₁ ligands on these cognitive tasks are reviewed. The results seen in the pre-clinical models are in accordance with the memory impairing effects of cannabis in humans. CB₁ agonists impair mnemonic performance in the delayed matching to position procedure, in the radial arm maze and in the Morris water maze task. All these effects could be blocked by the CB₁ receptor antagonist rimonabant. Furthermore CB₁ knock-out mice have been shown to possess enhanced memory in an object recognition task, are impaired in a reversal task in the water maze and show impaired extinction in a tone-shock fear conditioning paradigm. Treatment with the CB₁ antagonist rimonabant mimicked the phenotype of the CB₁ knock-out mice and in rats rimonabant enhanced social recognition and improved mnemonic performance in the eight arm radial maze. Taken together these data suggest that agonistic activity on the CB₁ system mediates extinction and the results from rimonabant indicate that a CB₁ antagonist diminishes extinction and therefore enhance long-term memory storage.