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. 2016 Dec 26;9:145. doi: 10.3389/fnmol.2016.00145

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Copyright © 2016 Francius, Hidalgo-Figueroa, Debrulle, Pelosi, Rucchin, Ronellenfitch, Panayiotou, Makrides, Misra, Harris, Hassani, Schakman, Parras, Xiang, Malas, Chow and Clotman.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Vsx1 identifies a population distinct from V2 interneurons. At e10.5 (A–A″) and e11.5 (B–B″), Vsx1 is present in cells that intermingle with, but are distinct from V2a (Chx10+) and V2b (Gata3+) interneurons. (C) Quantification of V2a, V2b and Vsx1⁺ cells at different stages (mean values ± SEM, n = 3). (D–D″) Vsx1 is not detected in V2d interneurons (Shox2 + Chx10−). (E) Vsx1⁺ cells are also distinct from V2c cells (Sox1+, arrow). (F–F″) At e10.5, OC-1 is present at low levels in Vsx1⁺ cells, while OC-2 is undetectable. (G–G″′) Ascl1 is present in Vsx1⁺ cells, confirming their p2 origin. Proteins present in V2a, including Prdm8 (G–G″′), Lhx3 and Bhlhb5 (H–H″′), are also detected. (I) In contrast, Lhx1/5, which is found in V2b, is barely detectable (arrowheads). Scale bars = 50 μm.