Figure 5
From: Time-controllable Nkcc1 knockdown replicates reversible hearing loss in postnatal mice
Changes in cochlear structure induced by DOX regulation of Nkcc1 expression. (a–g) Cochlear sections from mice at P35 observed with hematoxylin and eosin staining. (a,b) Cochlear structure in a control mouse. (a) Low-magnification view of cochlea from controls. Arrowheads: Reissner’s membrane; smaller arrow: SV region; larger arrow: SGNs. (b) Higher magnification view of cochlea of control. Arrows: point to the normal width and ordered structure in the control SV. (c) In one-third of WL-KD mice, Reissner’s membrane (arrowheads) adhered to the SV (smaller arrow), the endolymphatic space was collapsed, and SGNs (larger arrow) were sparse. (d–f) Higher magnification views of the variable morphology of SVs of WL-KD mice. The changes in the LW were not same among all mice. (d) In one-third of WL-KD mice, the SV (arrows) and the type II fibrocyte region (*) were atrophic and the endolymphatic space was collapsed. (e) In other mice, the acellular space was wider. Arrows point to the increased width and vacuolar-filled structure in the SV. (f) Atrophy of the SV was conspicuous even though the endolymphatic space was not collapsed. Arrows point to the empty narrowed structure in the SV. (g) In P0-KD adult mice, the cochlear structure did not differ from that of adult controls. (h–j) Surface preparations of cochleae from adult mice at P35. Phalloidin staining of actin (red) and Myo7a staining (green) were used to outline HCs. (h) Control mice had three regular rows of outer HCs and one row of inner HCs. (i) WL-KD mice showed degeneration of the organ of Corti and loss of HCs; remaining HCs were disorganized. (j) P0-KD mice showed only mild HC loss consistent with their partial hearing recovery. (k,l) IHC and OHC loss was considerably less in the basal turn than the apical turn in P0-KD mice.
