Chunk #20 — Results — Deleting Zfhx1b in SVZ of the MGE Using DlxI12b-Cre Phenocopies Loss of Zfhx1b function in the VZ (Nkx2.1-Cre) — Postnatal Analysis of cortical and striatal interneuron phenotypes in Nkx2.1-Cre;Zfhx1b mutants
We analyzed postnatal day 0 (P0) and P15 Nkx2.1-Cre;Zfhx1bF/- conditional mutants to better understand the nature and extent of their cortical and striatal interneuron defects. In the P0 neocortex there was an ~90% reduction in the number of EGFP+ Cre-reporter marked cells, as well as a decrease in Calbindin (CB), Sst, and Lhx6 expressing interneurons (Figures 4A-4C’; 4S). Likewise, at P15 there was a >90% reduction in number of neocortical EGFP+ cells (Figure 4D-4F’; 4S). Next, we counted the number cortical interneurons in the Nkx2-1-Cre lineage that expressed Parvalbumin (PV) or Sst, which are the two main MGE-derived subtypes (Rudy et al., 2011). We saw a strong reduction in double labeled neurons, with the numbers of EGFP+ interneurons expressing Sst or PV reduced by >90% or more (Figure 4S). The expression of cortical Calretinin (CR), which predominantly marks CGE-derived cortical interneurons, showed little to no change in the Zfhx1b; Nkx2.1-Cre conditional mutant (Figure 4F-F’).
