For cAMP assays, cells were treated similar to the N2A proliferat

For cAMP assays, cells were treated similar to the N2A proliferation assays; however, after 48 hr, cells were collected and cAMP levels were measured using a commercial kit (Promega). Immunoprecipation and western blot experiments were performed as described in Mao et al. (2009).

All images were acquired using a confocal Zeiss LSM 510 microscope. Images were further analyzed with Adobe Photoshop and ImageJ v1.42q. Statistical analysis was performed with the student’s t test. All bar graphs are plotted as mean ± SEM. We would like to thank Tsai lab members and Stanley Center members for helpful discussions. We would like to give a special thanks to Janice Kranz, Kimberly Chambert, Doug Ruderfer, Doug Barker, Jennifer Moran, and Edward M. Scolnick for their intellectual input and logistical support. check details L.-H.T. is an investigator of the Howard Hughes Medical Institute and the director of the neurobiology program at the Stanley Center for Psychiatric Research. K.K.S. is a recipient of the Human Frontiers Science Program Long-term fellowship and an NSERC postdoctoral

fellowship. Y.M. is a recipient of the National Alliance for Research on Schizophrenia and Depression Young Investigator Award. This work was partially supported by a NIH RO1 grant (MH091115) to L.-H.T. and a grant from the Stanley Center for Psychiatric Research to L.-H.T. “
“An abiding principle of brain organization holds that the precise synaptic connectivity of neuronal networks determines brain functions. Conversely, pathological disturbances of this neuronal and synaptic patterning may contribute to the symptomatology of many neurological and psychiatric illnesses. Farnesyltransferase click here Therefore, understanding molecular

mechanisms that regulate neuronal development and connectivity can generate insight into the processes that govern the functional integrity of the developing and adult brain. In the hippocampus of the adult mammalian brain, new neurons are continually generated from neural stem cells throughout the lifespan of the organism (Lledo et al., 2006, Ming and Song, 2005 and Zhao et al., 2008). Adult neurogenesis recapitulates the complete process of embryonic neuronal development, including proliferation and fate specification of neural progenitors, morphogenesis, axon and dendritic growth, migration, and synapse formation of neuronal progeny (Duan et al., 2008 and Ming and Song, 2011). Many signaling pathways play conserved roles during embryonic and adult neurogenesis and disruption of many of these same pathways have also been implicated in the etiology of psychiatric disorders (Harrison and Weinberger, 2005 and Kempermann et al., 2008). There is a growing body of evidence demonstrating a convergent effect of genetic mutations that both confer susceptibility to psychiatric diseases and result in dysregulation of neuronal development, supporting a neurodevelopmental origin of these diseases.

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