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Axotomy-induced retinal ganglion cell death in development: its time-course and its diminution by antioxidants
1Institute of Anatomy, University of Lausanne, Switzerland.
Abstract:
Developing neurons die when deprived of trophic support from their axonal target. Although this is generally attributed to the programmed expression of suicide proteins, recent data suggest that a less orderly mechanism involving oxidative stress may also be involved. We have studied retinal ganglion cell death in the chick embryo after a contralateral tectal lesion. The kinetics of cell death, as judged from counts of pyknotic cells, are described. In addition, we show that the pyknotic counts are reduced following intraocular injections of the protein synthesis inhibitor cycloheximide or the antioxidants N-t-butyl-alpha-phenylnitrone and N-acetyl cysteine. Our results suggest that target deprivation-induced ganglion cell death involves oxidative stress.
Insights
Neuronal death after target deprivation may involve oxidative stress, not just programmed cell death. Antioxidants and protein synthesis inhibitors reduced cell death in developing retinal ganglion cells.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Developing neurons require trophic support from their targets.
- Target deprivation typically induces programmed cell death via suicide proteins.
- Emerging evidence suggests oxidative stress may also contribute to neuronal death.
Purpose of the Study:
- To investigate the mechanism of retinal ganglion cell death following target deprivation.
- To determine the role of oxidative stress in this process.
Main Methods:
- Studied chick embryo model with contralateral tectal lesions to induce target deprivation.
- Quantified neuronal death by counting pyknotic cells.
- Administered intraocular injections of cycloheximide (protein synthesis inhibitor) and antioxidants (N-t-butyl-alpha-phenylnitrone, N-acetyl cysteine).
Main Results:
- Described the kinetics of cell death after tectal lesion.
- Observed a reduction in pyknotic cell counts after cycloheximide treatment.
- Demonstrated a decrease in pyknotic cell counts following antioxidant administration.
Conclusions:
- Target deprivation-induced retinal ganglion cell death involves oxidative stress.
- Inhibiting protein synthesis or applying antioxidants can mitigate this cell death.
- Suggests a significant role for oxidative stress mechanisms in developmental neuronal apoptosis.