Lack of p75 receptor does not protect photoreceptors from light-induced cell death

Exp Eye Res. 2003 Jan;76(1):125-9. doi: 10.1016/s0014-4835(02)00258-0.


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.

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / radiation effects*
  • Light / adverse effects*
  • Mice
  • Mice, Mutant Strains
  • Radiation Injuries / pathology*
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor / physiology*
  • Retinal Rod Photoreceptor Cells / radiation effects*


  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor