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Schizophrenia is a debilitating disorder which is often characterized by dysregulation of the processing of sensory information. Schizophrenia has been shown to have a strong genetic component, as well as a strong environmental component. As such, a number of hypotheses such as the diathesis stress hypothesis have been developed to explain the etiology of schizophrenia. As most of these theories attempt to account for a genetic and an environmental factor, they are often viewed as double-hit models of schizophrenia. Several theories have emerged as potential explanations for the symptoms of schizophrenia. The dopamine hypothesis suggests that the basal level of dopamine transmission within the mesolimbic and mesocortical pathways is increased in schizophrenia. The glutamate hypothesis suggests that increased glutamate transmission in the striatum combined with NMDA receptor hypofunction could result in some of the symptoms of schizophrenia. Both the dopamine and the glutamate hypothesis draw on the idea that individuals with schizophrenia show heightened neural activation as compared with non-schizophrenics. The developmental theory of schizophrenia posits that insults to the brain occurring during development may causes changes in the brain which result in the symptoms of schizophrenia later in life. In this study, CHL1 deficient mice, an animal model of schizophrenia were compared with their wild type littermates on measures of neuronal activation and latent inhibition, a measure of normal attentional and sensory processing. Additionally, some mice from both genotypes were selected to receive stress. It was found that all unstressed mice as well as the wild type stressed mice showed latent inhibition. The stressed CHL1 deficient mice did not show latent inhibition, the absence of which is associated with the positive symptoms of schizophrenia. These results provide support for a double hit (environment x genetic) account of schizophrenia.



Faculty Mentor

Catalin V. Buhusi

Departmental Honors Advisor

Scott Bates

Capstone Committee Member

Mona Buhusi