Inactivation in thalamus does not affect wiring, and joint inactivation in cortex and thalamus affects it mildly. At P0, hematoxylin–eosin (H&E) (A–D), neurofilament immunostaining (NF) (E–H), and protein kinase Cγ immunofluorescence (Prkcg) (I–L) show that, upon inactivation in thalamus using Foxb1-Cre (A, C, E, G, I, and K) (n = 5 and 3, respectively), the anterior commissure (AC), the IC (arrows in E and G), and the CST (arrows in I and K) are present. Joint inactivation in thalamus and cortex (n = 7 and 3, respectively) results in absence of AC crossing (B and D), atrophy of the IC (arrows in F and H) with some looping of axons close to the external capsule (arrowhead in F), and absence of CST in the spinal cord (J and L). These anomalies are similar to those obtained upon cortex-specific inactivation. [Scale bars: 500 µm (A–H); 200 µm (I–L).]