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Related Experiment Video

Updated: Feb 14, 2026

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Published on: April 25, 2011

Systemic Inflammation Aggravates Retinal Ganglion Cell Vulnerability to Optic Nerve Trauma in Adult Rats.

Giuseppe Rovere^1,2,3, Yolanda Caja-Matas^1,4, Beatriz Vidal-Villegas⁵

¹Department of Ophthalmology, Faculty of Medicine, University of Murcia and Biomedical Research Institute of Murcia (IMIB-Pascual Parrilla), 30120 Murcia, Spain.

International Journal of Molecular Sciences

|February 13, 2026

Summary

Systemic inflammation primes retinal microglia but doesn't cause cell death alone. However, it worsens neurodegeneration after optic nerve injury, highlighting microglia's role in retinal outcomes.

Keywords:

adult albino female rat inflammation lipopolysaccharide microglia activation microglial cells neuroinflammation optic nerve crush retina systemic infection traumatic injury

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Published on: April 25, 2011

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Partial Optic Nerve Transection in Rats: A Model Established with a New Operative Approach to Assess Secondary Degeneration of Retinal Ganglion Cells

Published on: October 15, 2017

Area of Science:

Neuroscience
Immunology
Ophthalmology

Background:

Systemic inflammation influences central nervous system neurodegeneration.
The role of systemic inflammation in retinal ganglion cell (RGC) survival and microglial responses after optic nerve (ON) injury is not fully understood.

Purpose of the Study:

To investigate the impact of systemic lipopolysaccharide (LPS)-induced inflammation on retinal microglial activation and RGC vulnerability.
To determine how systemic inflammation affects RGCs and microglia under physiological conditions and after traumatic ON damage.

Main Methods:

Adult female rats were administered LPS intraperitoneally.
Optic nerve (ON) crush was performed to induce injury.
Retinal microglial activation, proliferation, and RGC survival were assessed.

Main Results:

Systemic LPS induced rapid microglial activation and proliferation without causing RGC loss in intact retinas.
Following ON crush, systemic inflammation exacerbated late-phase RGC loss.
Increased microglial density and redistribution toward the ON head were observed in inflamed, injured retinas.

Conclusions:

Systemic inflammation primes microglia but does not directly cause RGC degeneration.
Inflammation amplifies neurodegeneration following axonal injury, with microglia playing a context-dependent role.
Modulating microglial activation may be a therapeutic strategy for optic neuropathies.