The study opens the doors to the design of drugs to improve the lives of patients with schizophrenia.
The University of the Basque Country (UPV / EHU) and the CIBERSAM of the Carlos III Institute have jointly identified the molecular-scale mechanisms involved in the increased risk of developing schizophrenia after consuming cannabis. In particular, the researchers have discovered the alterations that occur in the neurons of the cerebral cortex of mice treated chronically with THC (tetrahydrocannabinol). This study opens ways to generate prevention strategies, as well as the design of drugs and therapies to improve the lives of people with schizophrenia.
In the research, they have analyzed the brains of mice that began to administer THC chronically during the considered critical period for the development of their brain, which in people corresponds to adolescence. In the study of the cerebral cortex of these mice, researchers have detected alterations in the serotonin 2A receptor, the main responsible for the hallucinations characteristic of psychosis and schizophrenia. In particular, researchers have found that this receptor is increased its functionality after chronic treatment with cannabis.
The final aim of the study is to identify the existence of similar molecular changes in people who use cannabis to be able to relate them to the development of psychosis or schizophrenia. On the other hand, this research opens the way to the creation of new drugs that improve the symptomatology of patients with schizophrenia.
To carry out this study, the researchers used animal behavior techniques and, later, quantified proteins and receptors. The first showed that mice that had been treated with cannabis during “adolescence” had a greater predisposition to develop psychotic behaviors compared to control animals. In a next step, the research team marked and studied the serotonin 2A receptor and identified the signaling pathway through which an increased risk of suffering psychotic behavior could mediate.