and lead to increased schizophrenia risk (e.g. (Murray, Morrison, Henquet, & Di Forti, 2007)). A growing body of animal studies supports such a hypothesis. Chronic cannabis administration in adolescent rats, but not adult cannabinoid exposure, leads to enduring cognitive deficits in adulthood, including working memory deficits and prepulse inhibition abnormalities commonly observed in schizophrenia probands (O’Shea, McGregor, & Mallet, 2006; O’Shea, Singh, McGregor, & Mallet, 2004; Schneider & Koch, 2007). These persistent cognitive deficits are further associated with altered FOS protein expression within brain regions critical in schizophrenia (such as the hippocampus, nucleus accumbens, caudate and putamen)(Wegener & Koch, 2009).
