A progressive failure in phagocytosis by the retinal pigment epithelium (RPE) occurs in the Royal College of Surgeons rat with inherited retinal degeneration. Another change that can be attributed to a defect in the RPE is a breakdown in the blood-retinal barrier. RPE cell junctions, which form a part of this barrier, become permeable to extracellular tracer during the dystrophic process. We have used the freeze-fracture technique to study the structure of RPE cell junctions in normal and dystrophic retinas. In normal retinas, tight junctions between RPE cells consisted of 8 to 16 anastomosing strands on the cytoplasmic membrane leaflet (P-face) and a complementary pattern of groves on the external membrane leaflet (E-face). Gap-junctional aggregates of hexagonally packed P-face particles and complementary E-face pits were enclosed within the tight junctional strands. In dystrophic retinas changes were first seen at postnatal day 21. Subtle breaks in P-face tight-junctional strands became more pronounced with time. Eventually the tight junctions appeared to unravel from the gap junctional aggregates, which became isolated and appeared to break off into patches of particle aggregates. The increased density of background particles in the membranes adjacent to disassembling junctions suggested that junctional elements were being removed by dispersal. Endocytosis of junctional elements was observed in both dystrophic and control retinas but may be accelerated in the dystrophic retina. In the late stages of the dystrophy some RPE cell junctions appeared to have proliferated and occupied extensive areas of the RPE membrane.
|Original language||English (US)|
|Number of pages||14|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Jan 1 1982|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience