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The striavascularis in the aged, null mice was thinner than in the heterozygous or wildtype mice.
2
Cells expressing Sox10 were present in the striavascularis, outer sulcus and spiral prominence in mouse and human cochleas.
3
GR receptor mRNAs were demonstrated neither in cells of the striavascularis nor in cells of the organ of Corti region.
4
Immunoreactivity for sPLA2 also was detected in cultured marginal cells of the striavascularis and in fibrocytes of the spiral ligament.
5
We observed degeneration of striavascularis intermediate cells, the cells that generate the endocochlear potential, but no other abnormalities within the cochlea.
6
In the primate striavascularis, alpha B-crystallin was mainly seen in the basal cell layer and the adjacent cells of the connective tissue layer.
7
These results suggest that the striavascularis may be a site of the inner ear damage that follows bacterial inoculation into the middle ear cavity.
8
Transmission electron microscopy of the temporal bone revealed ultrastructural changes in the outer hair cells, striavascularis and cochlear ganglion at the cochlear basal turn.
9
We conclude that fluctuations of hearing result from fluctuations of the endocochlear potential and striavascularis dysfunction in Slc26a4-insufficient mouse ears.