At P15, the difference in expression was even more dramatic ( Figures 6C and 6D), with many fewer neurons expressing GFP in ThGVdKO mice, and these cells were largely distributed deeper in cortex, corresponding to L5a, than in control mice and did not express CUX1 ( Figure 6D). Thalamocortical axon terminal selleck chemicals llc arbors at P15 completely overlapped with the layer of neurons

expressing GFP ( Figure 6E), consistent with the dominant expression of Dcdc2a-Gfp in L4 of control mice. In contrast, in ThVGdKO mice, GFP neurons were present mainly below the bulk of thalamocortical axon terminal arbors ( Figure 6E). These data suggest that the normal maintenance in L4 and downregulation in L5a of Dcdc2a expression

are disrupted in ThVGdKO mice, possibly due to disruptions in postnatal neuronal position or changes in laminar expression of the Dcdc2a-Gfp reporter. We examined the expression of a number of genes with layer-specific expression patterns in ThVGdKO somatosensory cortex at P15 and consistently observed changes in and around L4. As already described, the expression of the predominantly superficial layer gene Cux1 in ThVGdKO mice was significantly reduced ( Figures 3G–3K), as was SatB2 ( Figures S5A and S5B). The expression of the L4 transcription factor Rorb (RORβ; Schaeren-Wiemers et al., 1997), and the L5a transcription factor Etv1 (aka Er81; Yoneshima et al., 2006), changed reciprocally

( Figures 7A–7D). In ThVGdKO, a dense band of Rorb-positive cells that corresponds to L4 was MDV3100 in vivo shifted upward ( Figures 7A and 7B), consistent with the Nissl staining ( Figures 3C and 3D). We also Oxalosuccinic acid observed a number of Rorb-positive cells throughout L5 and L6 in ThVGdKO mice, which was more unusual in controls ( Figure 7A, black arrows; Figures S6A and S6B, white arrows). In control mice, neurons expressing Rorb were mostly confined to L4 and coexpressed CUX1, whereas in ThVGdKO mice, Rorb expression extended to L5 where it was not coexpressed with CUX1 ( Figure S7). The domain of Etv1 expression spread toward the pial surface in ThVGdKO mice ( Figures 7C and 7D), again consistent with the expansion of L5 observed with Nissl staining. The expression of L5b (Ctip2, Fezf2) and L6 (FoxP2, Tbr1) markers was largely undisturbed in the somatosensory cortex of ThVGdKO mice ( Figures S5C–S5G, and data not shown), and changes in laminar-specific gene expression observed in somatosensory cortex did not occur in the motor cortex of ThVGdKO mice ( Figures S6C and S6D). None of these aberrant expression patterns were apparent at P6 ( Figure S6E). The changes in layer-specific gene expression observed in ThVGdKO cortex at P15 are consistent with the differences observed histologically and imply an unexpected degree of activity-dependent thalamic influence on laminar development of somatosensory cortex.