Abstract
The link between cannabis and psychosis has been debated although there is substantial epidemiological evidence showing that cannabis increases the risk of psychosis. It has been hypothesized that schizophrenia patients carrying particular risk genes might be more sensitive to the psychosis-inducing effects of cannabis than other patients and healthy test subjects. Here we review the effects of cannabinoids on a mutant mouse model for the schizophrenia candidate gene neuregulin 1 (Nrg1). The studies suggest a complex interaction between cannabis and Nrg1: the neuro-behavioral effects of cannabinoids were different in Nrg1 mutant and control mice and depended on exposure time, sex, and age of test animals. This research provides the first evidence of complex cannabis-Nrg1 interactions suggesting Nrg1 as a prime target for future clinical investigations. Furthermore, it highlights that animal model research can broaden our understanding of the complex multi-factorial etiology of schizophrenia. Finally, the findings are important to preventive psychiatry: if the genes that confer genetic vulnerability to cannabis-induced psychosis were identified patients at-high risk could be forewarned of the potential dangers of cannabis abuse.
Highlights
The two-hit hypothesis of schizophrenia states that a combination of genetic and environmental risk factors will cause the development of schizophrenia (Bayer et al, 1999; Rapoport et al, 2005; Caspi and Moffitt, 2006)
Neuregulin 1 (NRG1) is one of the more promising schizophrenia candidate genes as associations with schizophrenia have been found in several studies (Stefansson et al, 2002; Tosato et al, 2005; Munafo et al, 2006)
Similar to many other schizophrenia susceptibility genes, recent genome wide associations studies suggest that it is more important to consider an interplay of different genetic and environmental risk factors for schizophrenia to understand the etiology of the disorder (Sanders et al, 2008)
Summary
The two-hit hypothesis of schizophrenia states that a combination of genetic and environmental risk factors will cause the development of schizophrenia (Bayer et al, 1999; Rapoport et al, 2005; Caspi and Moffitt, 2006). Was treated with the main psychoactive component of cannabis ( 9-tetrahydrocannabinol: THC) during adolescence and exhibited a greater behavioral sensitivity to the long-term effects of THC (O’Tuathaigh et al, 2010) and a genotype-specific response in dopaminergic and GABAergic pathways as well as in the protein expression of cannabinoid 1 receptors (CB1) (Behan et al, 2012).
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