Figure 2.

Neocortical nNOS-expressing inhibitory neurons are derived from the medial ganglionic eminence. To ascertain and quantify the spatial origin of cortical nNOS inhibitory neurons, we employed different fate mapping strategies based on the use of Nkx2.1^Cre; RCE^EGFP (A), Lhx6^Cre; RCE^EGFP (B), or 5-Ht3a^EGFP mice (C). (A–C) Representative pictures of coronal sections of P21 mouse somatosensory neocortex immunolabeled with EGFP and nNOS. Fate mapped cells expressing EGFP and nNOS are indicated by arrowheads. Arrows indicated cells expressing nNOS only. (D,E) Histograms showing the fate mapping of cortical nNOS GABAergic neurons and the contribution of nNOS-expressing cells to MGE and CGE populations, expressed as the percentage of nNOS+/GFP+ cells in the entire nNOS positive population (D), or in the entire EGFP positive population (E). The Nkx2.1^Cre; RCE^EGFP fate mapping indicates that 28.5 ± 4.3% of nNOS GABAergic neurons originate from the MGE domain covered by the Nkx2.1^Cre driver line (A,D) and that nNOS cells account for 0.7 ± 0.2% of this Nkx2.1^Cre-derived population (A,E) (n = 3 independent brains). The Lhx6^Cre; RCE^EGFP and 5-Ht3a^EGFP fate mapping strategies revealed that virtually all nNOS-cINs originate from the MGE (93.0 ± 3.3%) (B,D) and not from the CGE (no cells co-express nNOS and GFP) (C,D), respectively (n = 3 independent brains for each genotype). On the other hand, nNOS cells account for 2.6 ± 1.1% of MGE-derived inhibitory neurons fate mapped by the Lhx6^Cre; RCE^EGFP (B,E). Data represent mean ± SEM. Scale bars correspond to 100 μm (A–C) and 25 μm (A1,B1,C1,C2).