Alterations in hippocampal neurogenesis have been implicated in SCZD (Tamminga et al., 2010). We have previously demonstrated a decrease in connectivity in SCZD neurons using a rabies virus (Brennand et al., 2011) but did not find a corresponding electrophysiological deficit. In addition, in our previous work, we used a single mature time point to examine these differences, not taking advantage of the temporal differentiation that can be measured in vitro. Thus, we used our hippocampal DG differentiation paradigm to model SCZD-associated defects in hippocampal neurogenesis as a proof-of-principle application. We applied the EB-based hippocampal differentiation approach to hiPSC lines previously derived from four SCZD patients and four control individuals (Brennand et al., 2011). From the panel of hippocampal neurogenesis markers that were assessed, we observed a trend for reduced expression levels of Emx2 and Pax6 (Figures 6A and 6B) in SCZD hiPSCs compared to control hiPSCs. However, the expression levels of NEUROD1 and PROX1 in the SCZD lines were significantly lower compared to the controls (Figures 6D and 6E). Furthermore, the expression of TBR1, a transcription factor found in postmitotic
