of PV interneuron dysfunction in schizophrenia (Lewis et al., 2005). Fast-spiking PV+ cortical interneurons are observed late during primate prenatal development and continue their maturation into early adulthood (Anderson et al., 1995; Insel, 2010). Given the important role of PV+ neurons under various pathological conditions our data suggest that disease modeling of such states may be feasible using our differentiation strategies. Another key for the future will be the development of protocols that allow the enriched generation of specific cortical interneuron subgroups such as somatostatin+ versus PV+ cells. Our previous results in MGE progenitors indicate that this decision may be yet again under control of SHH signaling, with higher levels promoting somatostatin+ and lower levels promoting PV+ neurons (Xu et al., 2010).
