Lack of p75 receptor does not protect photoreceptors from light-induced cell death.
Rod photoreceptors are susceptible to light-induced cell death. Previous results have suggested that the neurotrophin receptor p75 in Müller cells controls photoreceptor cell death during light-exposure by suppressing trophic factor release; and consequently, if p75 is blocked or eliminated during light-exposure, apoptosis is delayed. We explored this question by examining photoreceptor cell survival in albino p75(-/-) mice as well as their heterozygous and homozygous littermates. Photoreceptor cell death was examined in semi-thin sections by counting the remaining rows of photoreceptors. No difference in the amount of cell death was found between p75(+/+) and p75(-/-) animals, whereas the single copy of p75 in the heterozygous p75(+/-) mice provided significant neuroprotection. Cell death in the wild-type animals may indeed be mediated by p75, whereas other known apoptosis pathways may be activated in the p75(-/-) mice. The pro-apoptotic activity of the p75 receptor may have been partially suppressed in the heterozygous p75(+/-) mice by the silencing effect of the Trk receptor. Thus, our results suggest that p75 signaling does not mediate the main apoptosis pathway activated during light-damage.
Rohrer
B
B
Matthes
M T
MT
LaVail
M M
MM
Reichardt
L F
LF
D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D008027:Light / Q000009:adverse effects*; D051379:Mice; D008817:Mice, Mutant Strains; D011832:Radiation Injuries / Q000473:pathology*; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000502:physiology*; D017948:Retinal Rod Photoreceptor Cells / Q000528:radiation effects*
D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor