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Mitrofanis Pavlidis, Dietmar Fischer, Solon Thanos; Photoreceptor Degeneration in the RCS Rat Attenuates Dendritic Transport and Axonal Regeneration of Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2000;41(8):2318-2328.
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purpose. Photoreceptor loss in the Royal College of Surgeons (RCS) rat deprives
the retinal ganglion cells (RGCs) of sensory input, which could
interfere with RGC physiology. Whether axonal and dendritic transport
is altered, and whether RGCs retain their capacity to regenerate their
axons, both in vivo and in culture, was ascertained.
methods. The study was conducted at postnatal days (P) 30 (while most
photoreceptors are still intact), P90 (photoreceptors being almost
completely absent), and P180 (approximately 3 months after
photoreceptor disappearance). RGCs were studied with retrograde
transport of the fluorescent dye 4Di-10ASP. Dendritic transport was
also studied with 4Di-10ASP that is transported from the cell bodies
into the RGC dendrites. Regeneration of RGC axons in vivo was monitored
in the grafting paradigm of replacing the cut optic nerve (ON) with a
sciatic nerve (SN) piece. Cell counts were performed in retinal
wholemounts. Axonal regrowth in vitro was assessed in organotypic
cultures of retinal stripes.
results. Photoreceptor dystrophy did not adversely affect retrograde axonal
transport but attenuated dendritic transport compared with the
wild-type control rats. Axons of RGCs were able to regenerate if
provided with a SN graft, and regeneration was observed to be similar
between RCS and wild-type rats at P30 but differed significantly at P90
and P180. In addition to an age-dependent decline in the regenerative
ability, seen also in control animals, the number of RCS RGCs able to
regenerate declined drastically beginning at 3 months. It is plausible
that the intraretinal reorganization, as a consequence of photoreceptor
disappearance, interferes with the regenerative ability of the RGCs.
conclusions. The findings suggest for the first time that diminution of
photoreceptor sensory input does not induce detectable death of RGCs
until P180, but that it attenuates certain ganglion cell functions like
intraretinal dendritic transport and propensity for axonal
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