Figure 7.

Pou4f3 deletion affects SGN survival in the long term. Representative confocal images of mid-modiolar cryosections from control (A, C, E) and cochleae with Pou4f3 deletion at P0/P1 using Atoh1-Pou4f3cKO mice (B, D) or at 8 weeks using Prestin-Pou4f3cKO mice (F). All samples were analyzed at 4 months post-tamoxifen. SGN cell bodies were identified using Tuj1 immunostaining (green) in the middle turn of each cochleae. Representative images of neuronal fibers projecting to the organ of Corti from control (G, I), Atoh1 Cre-Pou4f3cKO (H) and Prestin Cre-Pou4f3cKO (J) cochleae after deletion of Pou4f3 at neonatal or adult ages. (K) Quantification of Tuj1-positive SGNs after deletion of Pou4f3 at neonatal and adult ages. N = 3. There was a significant main effect of genotype [F_(1,4) = 78.34, p = 0.0009]; age of Pou4f3 deletion [F_(1,4) = 15.84, p = 0.0164]; and an interaction between genotype and age of Pou4f3 deletion [F_(1,4) = 15.84, p = 0.0164]. Differences in the percentage of SGN loss between control samples and the respective age of deletion are indicated by the asterisks based on a Sidak's post-hoc test. OC, organ of Corti; RC, Rosenthal's canal. Scale bar = 20 μm.