(A) Schematic of the transgenic Pdgfrb-CreERT2/iDTR mouse model incorporating an inducible Cre-loxP system. (B) The diagram shows the timeline of tamoxifen and diphtheria toxin (DT) administration and the time point for tissue harvest. (C) Colocalization of Cre and PDGFR-β signals (green) is seen in the strial vasculature of Pdgfrb-CreERT2/tdTomato mice (middle right and right: low-magnification and high-magnification images, n = 4). (D) Pericyte density in the strial vasculature is significantly reduced in pericyte-depleted mice (n = 7) compared with control mice (n = 6) at the apical, middle, and basal turn (****P < 0.0001 by Student’s t test). (E) Total vascular density in the stria is also significantly reduced in pericyte-depleted mice (****P < 0.0001 by Student’s t test). (F) Maximum and minimum vessel diameter in control and pericyte-depleted animals (maximum diameter is approximately 12.9 ± 1.8 μm in control mice (n = 6, total 153 vessels analyzed), 16.2 ± 2.6 μm in pericyte-depleted mice (n = 7, total 180 vessels analyzed); minimum vessel diameter is approximately 4.6 ± 1.1 μm in control mice, 1.9 ± 0.8 μm in pericyte-depleted mice. (G–I) Representative figures show the capillaries of the stria in control (G) and pericyte-depleted mice 2 weeks after DT injection (arrows, H and I). The depletion of pericytes leads to some vessel enlargement (arrows, H) and shrinkage (arrows, I). (J and K) Albumin-FITC leakage was identified under IVM in pericyte-depleted mice (white arrows, K) but not in the control animals (J). (L) Statistical difference in vascular leakage between control and pericyte-depleted animals (n = 3, ***P < 0.001 by Student’s t test). Data are presented as mean ± SEM. Scale bars: 10 μm (C left, middle left, middle right), 30 μm (C right). 20 μm (G, H, I). 50 μm (J, K).