Ultrastructural examination was undertaken to investigate the pathogen
esis of age-related atrophy of the stria vascularis (StV). Basement me
mbrane (BM) thickness was increased in 65-85% of strial capillaries in
gerbils aged 33 months or older and often exceeded by several-fold th
at observed in young controls. In an early stage of thickening the BM
expanded slightly around the full capillary profile, after which nodul
ar expansions of BM encircling slender cell processes were often obser
ved at or near one or both poles of the elliptical vessel profile. As
widening progressed, the BM consisted of 2-3 layers separated by cell
processes in the nodules but fewer strata elsewhere. Association of sl
ender processes of both endothelial cells and pericytes with focal thi
ckening outside the process suggested their participation in genesis o
f the capillary lesion. In later stages of atrophy, pericytes degenera
ted and disappeared, while endothelial cells remained intact. Eventual
ly, thick multilayered BM devoid of endothelial cells surrounded a nar
row lumen occluded by debris. The age-related change in BM in the inne
r ear was confined to StV capillaries. Degenerative changes in StV epi
thelial cells occurred apparently as a secondary consequence of the ca
pillary lesion. The pathologic alterations in marginal cells included
extrusion of blebs from the luminal surface, separation and loss of ba
solateral interfoldings, alteration and depletion of mitochondria and
nuclear pyknosis. At the end-stage of degeneration, the StV consisted
of a simple or multiple layer of squamous cells lining the scala media
.