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Latent inhibition is an attentional phenomenon under which conditioning to a given stimulus is retarded upon repeated stimulus presentation [1]. Interestingly, latent inhibition is impaired in individuals with schizophrenia as compared with individuals without schizophrenia. The close homolog to L1 (CHL1) gene has been linked to the genetic predisposition to f schizophrenia [2]. Mutations in the CHL1 gene are known to affect brain development, particularly neuronal migration and development of neuronal connections, as well as cellular signaling pathways [3,4,5]. In this experiment CHL1 knockout (KO) and wild type (WT) mice received six weeks of chronic mild stress (CMS). We hypothesized that CMS might bring about the onset of schizophrenia-like behaviors in the KO mice. The mice were tested behaviorally in a latent inhibition paradigm, then sacrificed for histology. c-fos immunohistochemistry stainining was performed to assess neuronal activation; c-fos is a gene encoding a transcription factor which is transcribed immediately following neuronal activity (immediate early gene), making it a useful tool to observe differences in activation in the context of specific behaviors. Neural activation in several brain regions involved in latent inhibition was analyzed and results were compared between the different genotypes and behavioral groups. Brain regions were selected based upon the known circuitry of the latent inhibition network, a diagram of which can be seen below.

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