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Updated: Aug 6, 2026
Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System
Published on: May 12, 2011
Examination of cellular and molecular events associated with optic nerve axotomy
Anat Nitzan1, Pawel Kermer, Anat Shirvan
1Goldschleger Eye Research Institute, Chaim Sheba Medical Center, Tel Hashomer, Israel.
Purpose:
Analyzing cellular behavior during scar formation and determining the expression of growth inhibiting molecules in the optic nerve and retina following acute optic nerve injury.
Methods:
A rat model of complete transection of the optic nerve that spares the vascular supply and the neural scaffold was used. The response of the optic nerve and retinas to axotomy was studied by immunological and biochemical approaches.
Results:
Optic nerve axotomy led to massive cell invasion at the site of injury that spread along both sides of the nerve. The cells were microglia, oligodendrocytes, and to a lesser extent astrocytes. A marked induction of semaphorin 3A was evident, especially in the area of the scar, and persisted up to the 28th day of the experiment. Expression of neuropilin-1, a component of the semaphorin 3A receptor, increased following injury. The molecular events associated with axotomy were studied by measuring the levels of semaphorin 3A, p38 MAPK, and ERK1/2 in the retina. Semaphorin 3A levels and the activated form of p38 were elevated 3 days post-axotomy and then declined; ERK1/2 activation levels reached their peak 14 days post axotomy. Acute nerve injury led to morphological alterations in oligodendrocytes, astrocytes, and the extracellular matrix, disrupting the delicate internal organization of the optic nerve.
Conclusions:
We suggest that cell invasion, semaphorin 3A and neuropilin-1 induction, and disruption of the internal organization of the optic nerve contribute to axotomy-induced degenerative processes.
Insights
Optic nerve injury triggers cell invasion and the upregulation of growth inhibitors like semaphorin 3A, contributing to nerve damage. This study details the cellular and molecular responses to optic nerve axotomy.
Area of Science:
- Neuroscience
- Cell Biology
- Ophthalmology
Background:
- Scar formation after optic nerve injury is a complex process involving cellular responses and molecular signaling.
- Understanding these responses is crucial for developing therapeutic strategies to promote optic nerve regeneration.
Purpose of the Study:
- To analyze cellular behavior during scar formation in the optic nerve and retina after injury.
- To determine the expression of growth-inhibiting molecules following acute optic nerve injury.
Main Methods:
- Utilized a rat model of complete optic nerve transection, preserving vascular supply and neural scaffold.
- Employed immunological and biochemical approaches to investigate the response of the optic nerve and retina to axotomy.
Main Results:
- Optic nerve axotomy induced significant cell invasion (microglia, oligodendrocytes, astrocytes) at the injury site.
- Demonstrated marked induction of semaphorin 3A and increased neuropilin-1 expression post-injury, persisting for 28 days.
- Observed alterations in semaphorin 3A, p38 MAPK, and ERK1/2 activation, alongside morphological changes in neural cells and the extracellular matrix.
Conclusions:
- Cellular invasion, semaphorin 3A/neuropilin-1 induction, and structural disruption contribute to optic nerve degeneration after axotomy.
- These findings highlight key molecular and cellular events implicated in the failure of optic nerve repair.
