A comparative survey of synaptic changes in the rod photoreceptor terminals of rd, rds and double homozygous mutant mice.
In the developing retina of homozygous rd/rd mutant mice the time of onset of degenerative changes and the period of rapid photoreceptor cell loss overlaps the later phase of differentiation during which the maturation of the receptors and the completion of the synaptic connections take place. It remains unresolved if the retarded synaptogenesis within the photoreceptor terminals of the rod cells is a direct effect of the mutant gene or an indirect consequence of premature cell death. In the retina of homozygous rds/rds mutant mice early indication of gene expression within the photoreceptor cells is also recorded as photoreceptor outer segments fail to develop. However, during the very slow rate of degeneration, the surviving cells develop normal synaptic contacts within their terminals. Furthermore, some of the rod cells, though not the cones, go on to enlarge their synaptic structures as more and more photoreceptor cells are lost. In the retina of double homozygous mutant rd/rd;rds/rds mice the photoreceptor cells remain lacking in outer segments, as would be expected, but curiously enough, survive longer than in the rd/rd retina. Among this population of photoreceptor cells with extended life-span profiles of rod terminals are frequently encountered which contain a normal synaptic structure - one synaptic ribbon with two laterally placed processes of horizontal cells and one medially facing process of a bipolar cell. A number of these terminals also show signs of synaptic enlargement. Thus it can be concluded that some of the terminals of the rod photoreceptor cells of the double homozygous rd/rd,rds/rds mice, which survive longer than in the rd/rd mice, develop synapses that are either comparable to normal or resemble those of the rds/rds retina. These findings suggest that retarded synaptogenesis within the rod terminals of the rd/rd retina is likely to result from a pathogenic defect affecting the whole cell and is not due to a specific or exclusive action of the mutant gene on the synaptic components involved.
Sanyal
S
S
Department of Anatomy, Faculty of Medicine, Erasmus University, Rotterdam, The Netherlands.
Jansen
H
H
D000818:Animals; D005838:Genotype; D006720:Homozygote; D051379:Mice; D008809:Mice, Inbred C3H; D008817:Mice, Mutant Strains; D010786:Photoreceptor Cells / Q000254:growth & development / Q000473:pathology*; D012162:Retinal Degeneration / Q000235:genetics / Q000473:pathology*; D012374:Rod Cell Outer Segment / Q000254:growth & development / Q000473:pathology* / Q000648:ultrastructure; D013569:Synapses / Q000473:pathology*