New Perspectives in the Studies on Endocannabinoid and Cannabis: Cannabinoid Receptors and Schizophrenia
Hiroshi Ujike, Yukitaka Morita
Journal of Pharmacological Sciences 2004 DOI: 10.1254/jphs.fmj04003x4 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Review Peer reviewed |
|---|---|
| Topics | Cannabis |
| Citations | 94 |
| Key findings | Reviews evidence that cannabis use is linked to psychosis and schizophrenia, with recent biological and genetic findings indicating increased CB1 receptor density in prefrontal cortex, elevated anandamide in CSF, and an association between the CNR1 gene and schizophrenia, especially hebephrenic type. Individuals with a 9-repeat allele may have 2.3-fold higher susceptibility. The authors propose that central cannabinoid system hyperactivity is involved in schizophrenia pathogenesis or negative symptom mechanisms. |
Abstract
Cannabis consumption may induce psychotic states in normal individuals, worsen psychotic symptoms of schizophrenic patients, and may facilitate precipitation of schizophrenia in vulnerable individuals. Recent studies provide additional biological and genetic evidence for the cannabinoid hypothesis of schizophrenia. Examinations using [3H]CP-55940 or [3H]SR141716A revealed that the density of CB1 receptors, a central type of cannabinoid receptor, is increased in subregions of the prefrontal cortex in schizophrenia. Anandamide, an endogenous cannabinoid, is also increased in the CSF in schizophrenia. A genetic study revealed that the CNR1 gene, which encodes CB1 receptors, is associated with schizophrenia, especially the hebephrenic type. Individuals with a 9-repeat allele of an AAT-repeat polymorphism of the gene may have a 2.3-fold higher susceptibility to schizophrenia. Recent findings consistently indicate that hyperactivity of the central cannabinoid system is involved in the pathogenesis of schizophrenia or the neural mechanisms of negative symptoms.