Genome wide linkage studies, case-control association studies, and functional data suggest a role forNeuregulin 1 (NRG1) in the e'tiology of schizophrenia. Developmental studies indicate that defects in NRG1signaling mediated through its receptor, ErbB4, could lead to the incorrect generation, placement,differentiation, and function of neurons in the developing brain (Corfas et al., 2004). The resultant changes inneural circuitry in the cerebral cortex may thus lead to neurodevelopmental disorder such as schizophrenia.Recent evidence indicating that altered NRG1-erbB4 interactions may enhance susceptibility toSchizophrenia (Norton et al.,2005; Hahn et al.,2006) and that NRG1(I) expression is deregulated indorsolateral prefrontal cortex and hippocampus in schizophrenia (Hashimoto et al 2004; Law et al., 2006)further support this hypothesis. Therefore, an understanding of the functions of NRG1 and erbB4 receptorsin the developing cerebral cortex, especially during interneuronal development, is essential to delineate theneurodevelopmental pathways whose disruption is likely to be integrally related to the development ofschizophrenia. We propose to accomplish this by examining the following three related questions: (i)Determine the patterns of migration and positioning of interneurons in the embryonic cerebral cortex, (2)Determine whether the development and differentiation of interneurons, during early embryonic developmentand postnatally, depends on NRG1- ErbB4 interactions, and (3) Determine the role of ErbB4 in the functionof cortical interneurons..

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National Institute of Mental Health (NIMH)
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University of North Carolina Chapel Hill
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