Schizophrenia is a highly disabling disease that affects 1% of the population, which would involve an imbalance in the dopaminergic neurotransmission and a glutamatergic hypofunction. The Delta9-tetrahydrocannabinol (Delta9-THC), the main psychotomimetic constituent of Cannabis sativa, induces psychotic reactions and cognitive changes similar to schizophrenia symptoms. However, canabidiol, another component of cannabis, devoid of psychotomimetic properties and has been described as a compound with possible antipsychotic profile. Clinical studies have investigated the use of cannabidiol as an alternative treatment for schizophrenia and reported its therapeutic effects. Until now, few preclinical studies have been performed to support or refute the clinical utility of cannabidiol as an antipsychotic and to identify its mechanism of action and properties. Sensorimotor deficit characterized by prepulse inhibition (PPI) disruption is presented by schizophrenia patients and is reproducible in the lab. The aim of this study is first to investigate the ability of canabidiol to reverse the amphetamine effects in predictive models for antipsychotics action that reproduce positive, negative and cognitive schizophrenia symptoms (PPI, social interaction and object recognition), second, to investigate the nucleus accumbens relevance on canabidiol effects, and finally, to evaluate c-Fos protein expression as a measure of the mesolimbic regions possibly involved in the cannabidiol effects.
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