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Chunk #24 — 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

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Dlx1&2-dependent expression of Zfhx1b (Sip1, Zeb2) regulates the fate switch between cortical and striatal interneurons.
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Despite the cell death, Zfhx1b conditional mutants at P15 continued to have significantly increased numbers of striatal nNOS, NPY, Sst and TacR1 expressing cells (183%, 230%, 225%, and 164%; Figures 4N-4Q’, 4T). Importantly, total striatal PV+ cells were decreased by 58% (Figure 4S). Furthermore, there was no detectable change in TrkA expression (Figure 4R-4R’, 4T), which marks striatal cholinergic interneurons. We saw very few CR+ cells in the control striatum (1-3 cells per section), which did not noticeably change in the Zfhx1b conditional mutant (data not shown). Thus, Nkx2.1-Cre;Zfhx1b mutants have a selective increase in striatal interneurons expressing nNos, NPY, Sst and TacR1, but have reduced PV interneurons, and no change in cholinergic or CR interneurons.