Morphology of the stria vascularis. Hematoxylin-eosin staining of the stria vascularis at the cochlear basal turn in Irs2+/+Ptpn1+/+ (A–D), Irs2−/−Ptpn1+/+ (G–J) and Irs2−/−Ptpn1−/−mice (M–P) at 5 wks (left column) and 11 wks (right column) of age is shown. Wild-type mice showed normal morphology, vasculature pattern and thickness (bracket) of the stria vascularis (A–D). (B, D) Amplified detail of the stria vascularis illustrating the three epithelial layers, the basal, the intermediate and the marginal cell layers and the normal capillary network. Irs2−/−Ptpn1+/+ mice present numerous intercellular spaces, probably because of degeneration of the marginal cells (arrows) and the merging of the capillaries (dashed arrows) (G-J). At postnatal wk 5, Irs2−/−Ptpn1−/− mice show a slight atrophy of the stria vascularis with few intercellular spaces (dashed arrows) (M and N). The degeneration process worsens with age and 11-wk-old double-null mice show severe atrophy and a number of merged capillaries (dashed arrows) (O, P). (E, F, K, L, Q, R) Laser confocal microscopic examination showing Kir4.1 immunoreactivity (red). In control mice, immunostaining appeared as a fold-like structure at the basolateral side of marginal cells, designating the normal invaginations of these cells (dotted white line in E and F). Both mutant mice show a significant reduction in Kir4.1 expression and an irregular shape of the invaginations of the marginal cells (dotted white line in K, L, Q and R). B, basal cells; C, capillary network; I, intermediate cells; M, marginal cell; StV, stria vascularis. Scale bars: A, C, G, I, M, O: 50 µm; B, D, H, J, N, P: 25 µm; E, F, K, L, Q, R: 25 µm.