Effects of SNI on synaptic connectivity and BDNF expression are prevented by genetic deletion of TNFR 1. A, B, Representative images of biocytin-labeled CA1 pyramidal neurons (A) and their indicated dendritic length (B) (n = 12, basal, p = 0.361; apical, p = 0.335), branch number (n = 12, basal, p = 0.395; apical, p = 0.605), and Sholl analysis (n = 12, p = 0.231) in TNFR1 KO mice from the sham and SNI groups. C, Representative images and summary data of dendritic spine densities of CA1 neurons in the indicated groups (n = 12, basal, p = 0.406; apical, p = 0.369). Twelve neurons from six mice per group were used for the morphological analysis. D, E, Representative images and the summary data of dendritic length (n = 14, p = 0.234), branch number (n = 14, p = 0.394), and Sholl analysis of spinal NK1-PNs in sham and SNI groups of TNFR1 KO mice (n = 14, p = 0.320). F, Representative images and summary data of dendritic spine densities of spinal NK1-PNs in the indicated groups (n = 14, p = 0.234). Fourteen neurons from six mice per group were analyzed. G, Western blots showing the level of BDNF in contralateral (C) and ipsilateral (I) hippocampus or spinal dorsal horn of TNFR1 KO mice in sham and SNI groups: hippocampus, n = 5, p = 0.422 (C), p = 0.485 (I); spinal dorsal horn, n = 5, p = 0.298) (C), p = 0.372 (I). Data for all bar graphs were analyzed using Student's t test. Data for graphs in which Sholl analyses is plotted were analyzed using repeated-measures two-way ANOVA.