Figure 7
From: Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline

Abrogation of neocortical DCC expression fails to reproduce the abnormal pyramidal decussation observed in Dcc kanga/− mice. (A) Schematic representation of a sagittal section through an adult mouse CNS indicating the trajectory of the CST and the level of the coronal sections presented in this figure. Biotin dextran amine (BDA) was injected into the left motor cortex of Dcc +/+ (n = 4; B–E, B’–E’), Dcc kanga/− (n = 4; F–I; F’–I’) and Emx1::cre;Dcc lox/lox (n = 3; J–M, J’–M’) mice to label the left-sided CST axons. The CST was visualized on coronal sections at the level of the pyramidal decussation and in the spinal cord, by immunostaining against the PKCγ (visualization of the two CSTs; B–M), or by revelation of the BDA tracer (visualization of the left-hand CST alone; B’–M’). The CST trajectory was similar in Dcc +/+ (B–E) and Emx1::cre;Dcc lox/lox (J–M) mice. In Dcc kanga/− mice, the CST axons did not cross the midline at the pyramidal decussation, but spread in two bundles, one lateral and the other medial, that remained in the ventral ipsilateral spinal cord (F–I). The scale bar represents 336 μm in B, C, F, G, J, K; 168 μm in E, I, M; and 84 μm in D, H, L.