Figure 2. MGE Corridor Cells Derive from the LGE and Are Permissive for TCAs Outgrowth.

(A–D) Coronal sections through the telencephalon of E11.5 (A and C) and E12.5 (B and D) embryos showing the expression pattern of Ebf1 (A and B) and double immunohistochemistry Islet1 and βIII-tubulin (C and D).

(E) Experimental paradigm used to test the origin of corridor cells.

(F) GFP immunohistochemistry showing LGE-derived cells in the striatum (solid arrowhead), neocortex (NCx), and MGE mantle (open arrowhead).

(G) Higher magnification of LGE-derived GFP cells forming a stream superficial to the globus pallidus (GP).

(H and I) Migratory morphology of GFP cells at the MGE corridor (H). Most of them express Islet1 (I, open arrowheads).

(J) Experimental paradigm used to block cell migration between the LGE and MGE.

(K and L) Expression of Islet1 in control (K) and experimental slices (L). Note that the membrane (delineated by arrows) does not affect Islet1-positive cells in the POa. Arrows in (K) indicate the location of the control incision.

(L') Double immunohistochemistry for Islet1 and Nkx2-1 in the same slice shown in (L).

(M) Experimental paradigm used to test the growth of E13.5 GFP dorsal thalamic (dTh) in the MGE.

(N) Bright-field image of a slice with a GFP dTh explant in the POa after 72 hr in culture.

(O and P) Islet1 and GFP immunohistochemistry showing that TCAs grow preferentially through the MGE Islet1-positive corridor (open arrowhead, bracket in [P]) before fanning out in the striatum (Str; solid arrowheads). VZ/SVZ, ventricular/subventricular zone. Scale bars = 100 μm (A, C, and O), 200 μm (B, D, K, L, L', and N), 300 μm (F), 60 μm (G), 20 μm (H and I), and 70 μm (P).