Cortical interneurons are important for balancing excitation and inhibition within cortical circuitry and play critical roles in controlling developmental plasticity. Cortical interneuron dysfunction has been implicated in various pathological conditions such as epilepsy, autism or schizophrenia (Baraban et al., 2009; Insel, 2010; Lewis et al., 2005; Penagarikano et al., 2011). Our data demonstrate that day 10-18 treated cells express cortical interneuron progenitor markers such as OLIG2, MASH1, and NKX6.2. At day 18 of differentiation NKX2.1+ cells exhibit progenitor cell properties based on Nestin and Ki67 expression. Prolonged culture in the absence of extrinsic SHH activation led to a gradual decrease in Ki67 expression (Figure 3A–C, upper panels) and increased percentages of cells expressing the neuronal precursor markers DCX and TUJ1 (Figure 3A–C, lower panels). In addition, many GFP+ cells in the 10-18 and 2-18 conditions express GABA and subsequently calbindin (Figure 3A–C, lower panels), a marker of tangentially-migrating cortical interneuron precursors (Anderson et al., 1997). Importantly, western blot analysis at day 32 showed that LHX6 protein, a marker of post-mitotic, migratory cortical interneuron precursors in the mouse, was selectively enriched
