Although the association between adolescent marijuana use and subsequent schizophrenia is well-replicated, the nature of this relationship remains widely debated (e.g. (Henquet & Van Os, 2008)). The neurobiological mechanisms underlying how early adolescent cannabis exposure may confer increased schizophrenia susceptibility is poorly understood (D’Souza, Sewell, & Ranganathan, 2009; DeLisi, 2008; Kumra, 2007; Sewell, Ranganathan, & D’Souza, 2009). Most schizophrenia patients have no history of adolescent marijuana use, and the majority of adolescents who abuse marijuana do not go on to develop schizophrenia. Some have argued against a causal link (Degenhardt, Hall, & Lynskey, 2003; Hickman et al., 2009), and suggest that individuals with incipient schizophrenia may be self-medicating with marijuana. Other researchers have suggested that adolescence is a sensitive time period during which the brain may be especially vulnerable to deleterious effects of marijuana, which may disrupt normal brain maturation 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
