(A) Morphological characterization of biocytin filled CeA neurons from WT mice (P6 and P10) and P21 Grik1 cKO mice, injected with GFP-CRE or GFP (control) encoding AAV viruses to the BLA at P2-4. Example images and pooled data [P6 n = 8 (3); P10 n = 10(3); P21 GFP n = 11(4); P21 GFP-CRE n = 13(4)] illustrate developmental increase in spine density from P6 to P10 and from P10 to P21 in control mice (ANOVA F(3,38)=9.59, p<0.001; Holm-Sidak post-hoc comparison, P6 vs P10 t = 2.567, p=0.014; P10 vs P21 GFP t = 2.803, p=0.008). Following GluK1 inactivation, the spine density at P21 remains similar to P10 WT (Holm-Sidak, P6 vs P21 CRE t = 2.298, p=0.027; P10 vs P21 CRE: t = 0.441, p=0.662). **p<0.01. Scale bar, 5 µm. The n number refers to the number of experiments, followed by the number of animals in brackets. (B) Sholl analysis of the same neurons. The number of dendritic intersections and the total dendritic length is significantly increased during development from P6 to P21 in control mice (two-way ANOVA for dendritic intersections, F(19,418)=2.89, p<0.0001). Following GluK1 inactivation, the mean dendritic length and branching at P21 remains similar to P6–P10 WT’s (dendritic length, ANOVA F(3,35) = 5,724, p=0.003; Holm-Sidak post-hoc comparison P6 vs P10, t = 1.702, p=0.098; P10 vs P21 GFP, t = 1.771, p=0.085; P6 vs P21GFP t = 3.371, p=0.002; P6 vs P21CRE, t = 0.011, p=0.991; P10 vs P21CRE t = 1.835, p=0.075. Dendritic intersections, P10 vs P21CRE, two-way ANOVA F(11,240)=0.728,p=0.71). Confocal images (z-stack) illustrating the morphology of the dendritic tree. **p<0.01. Scale bar, 50 µm.