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Updated: Aug 3, 2026

Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System
Published on: May 12, 2011
Apoptosis in the developing visual system
A Cellerino1, M Bähr, S Isenmann
1Istituto di Neurofisiologia del CNR, Pisa, Italy.
Abstract:
Programmed cellular death is a widespread phenomenon during development of the nervous system. Two classes of molecules are particularly important in the context of apoptosis control in the nervous system: intracellular effectors homologous to the Caenorhabditis elegans Ced-3, -4, and -9 proteins, which in mammals correspond to the proteases of the caspase family, Apaf-1, and the members of the Bcl-2 protein family, and neurotrophic factors. Retinal ganglion cells lend a convenient model system with which to investigate apoptosis in central neurons during development as well as after injury. In this review, we discuss the role of these molecules in the control of programmed cellular death in the retinotectal system. Transgenic animal models and expression studies have shown that caspases, Bcl-2, Bax, and possibly Bcl-X are necessary players for the control of programmed cellular death in retinal ganglion cells. Bax and caspase 3 expression in retinal ganglion cells is upregulated after injury, and inhibition of Bax or caspase 3 increases the survival of injured retinal ganglion cells. Neurotrophins can support the survival of injured retinal ganglion cells, but this effect is transient. The physiological role of neurotrophins in the development of the retinocollicular system seems more related to the topographic refinement of retinocollicular projections, a process that is mediated, at least partially, by selective elimination of retinal ganglion cells making inappropriate topographic projections.
Insights
Programmed cell death in the nervous system involves caspases and Bcl-2 family proteins. Inhibiting Bax or caspase 3 promotes retinal ganglion cell survival after injury.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Programmed cell death (apoptosis) is crucial for nervous system development.
- Key regulators include caspases, Bcl-2 family proteins, and neurotrophic factors.
- Retinal ganglion cells (RGCs) serve as a model for studying neuronal apoptosis.
Purpose of the Study:
- To review the roles of apoptosis regulators in RGCs within the retinotectal system.
- To explore the impact of injury on RGC apoptosis and survival.
- To examine the function of neurotrophins in RGC development and survival.
Main Methods:
- Review of transgenic animal models and expression studies.
- Analysis of RGC apoptosis and survival mechanisms.
- Investigation of neurotrophin effects on RGCs.
Main Results:
- Caspases, Bcl-2, Bax, and Bcl-X are essential for RGC apoptosis control.
- Bax and caspase 3 expression increase in RGCs post-injury.
- Inhibiting Bax or caspase 3 enhances injured RGC survival.
- Neurotrophins offer transient survival support to injured RGCs.
Conclusions:
- Bax and caspase 3 are critical for RGC apoptosis, with therapeutic potential.
- Neurotrophins primarily influence topographic refinement through selective RGC elimination.
- Understanding these pathways is key for neuroprotection and developmental studies.
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