A, Three-dimensional reconstructions of RCs from P20 wild-type (A1), Egr3(−/−) (A2), and mlcNT3(+/−) (A3) mice. VGLUT1-IR contacts (dots) are plotted on the dendrites of the traced cells. B, Estimates of VGLUT1-IR contacts per 10 μm of linear dendrite on CB-IR RCs of wild-type, Egr3(−/−) and mlcNT3(+/−) mice of P15 (light grey bars), P20 (black bars) and adult (dark grey bars) postnatal ages. Renshaw cells from wild-type animals show densities and changes with maturation similar to those reported in Mentis et al. (2006) and Siembab et al. (2010). In wild-type and Egr3(−/−) animals, RCs display statistically significant decreases in VGLUT1-IR contact density from P15 to adult (p<0.001, one-way ANOVA). In contrast, VGLUT1-IR contact density increased significantly from P15 to adult in mlcNT3(+/−) mice (p=0.041, one-way ANOVA). Compared to their age-matched wild-types, RCs in Egr3(−/−) animals always had statistically significant lower density of VGLUT1-IR contacts, while in mlcNT3(+/−) mice show significant increases: Lines indicate statistical comparisons at P15 (continuous line), P20 (dotted line), adult (dashed line)(asterisks indicate significance; p<0.05 in post-hoc Dunn’s comparison). In mature mlcNT3(+/−) mice (P20 and adult), VGLUT1-IR contact density on RCs more than doubled compared to wild-types. During postnatal maturation VGLUT1-IR densities significantly decreased in wild-types and Egr3(−/−) mutants and increased in mlcNT3(+/−) mice (p<0.001 One-Way ANOVA on Ranks). C, Densities recorded in three different Sholl bins (aerial distance from the center of the cell body) of 50 μm distances. The densities (within each genotype) were not significantly different among the three different Sholl bins, indicating that the changes in VGLUT1-IR contact density were equally distributed throughout the proximal dendrite.