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Updated: Jun 11, 2026

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
Published on: February 15, 2022
Altered calcium signaling in an experimental model of glaucoma
Minna Niittykoski1, Giedrius Kalesnykas, Kim P Larsson
1Department of Ophthalmology, University of Kuopio, Kuopio, Finland. mijoni@gmail.com
Purpose:
To investigate calcium signaling in a rat experimental model of glaucoma.
Methods:
A method for labeling ganglion cell layer (GCL) neurons with the calcium indicator Fura-2 in flat-mounted retinas of adult rats was established. Pharmacologically evoked responses in laser-induced glaucomatous and control retinas were imaged 2 weeks after the initial laser treatment. The optic nerves of the same eyes were evaluated for neurodegenerative changes.
Results:
After laser treatment, intraocular pressure (IOP) was elevated 1.5- to 4.9-fold (24.70 ± 15.57 mm Hg) compared with control eyes (8.71 ± 1.53 mm Hg), and the area of neurodegenerative axons in optic nerve sections of laser-treated eyes was increased by 1.2- to 13.3-fold. The basal intracellular Ca(2+) level, as revealed by the Fura-2 ratio, was elevated in GCL neurons of laser-treated eyes compared with controls. This might suggest a mild degree of damage at the level of the soma in the GCL neurons of eyes with elevated IOP. Although glaucomatous GCL neurons remained functional as assessed pharmacologically, analysis of imaging data revealed that responses evoked by a brief application of ATP were slightly reduced rather than increased in the cells of laser-treated eyes compared with controls. No significant relationships were found between IOP/optic nerve damage and functional characteristics (basal intracellular Ca(2+) level or response to carbachol/elevated K(+)/ATP) within cells of laser-treated eyes.
Conclusions:
Ca(2+) imaging is a useful tool to map altered physiological characteristics of individual GCL neurons in the glaucomatous eye.
Insights
Calcium signaling in ganglion cell layer (GCL) neurons was investigated in a rat glaucoma model. Elevated intracellular calcium and altered responses to ATP were observed in glaucomatous eyes, suggesting GCL neuron damage.
Area of Science:
- Neuroscience
- Ophthalmology
- Physiology
Background:
- Glaucoma is a leading cause of irreversible blindness.
- Optic nerve damage and ganglion cell layer (GCL) dysfunction are hallmarks of glaucoma.
- Understanding cellular signaling in glaucoma is crucial for developing effective treatments.
Purpose of the Study:
- To investigate calcium (Ca2+) signaling dynamics in GCL neurons within an experimental rat model of glaucoma.
- To establish a method for visualizing Ca2+ activity in GCL neurons of ex vivo retinas.
- To assess the functional consequences of elevated intraocular pressure (IOP) on GCL neuron physiology.
Main Methods:
- Developed a Fura-2 based calcium indicator labeling method for rat GCL neurons in flat-mounted retinas.
- Induced experimental glaucoma via laser treatment, creating elevated IOP and optic nerve damage.
- Imaged pharmacologically evoked Ca2+ responses in GCL neurons from glaucomatous and control retinas.
Main Results:
- Laser treatment successfully induced elevated IOP and significant optic nerve neurodegeneration in rats.
- Basal intracellular Ca2+ levels were elevated in GCL neurons of glaucomatous eyes, indicating potential soma damage.
- While GCL neurons remained functional, ATP-evoked responses were slightly reduced in glaucomatous versus control eyes.
Conclusions:
- Calcium imaging provides a valuable tool for characterizing physiological alterations in individual GCL neurons in glaucoma.
- The study demonstrates altered calcium signaling in GCL neurons in a rat model of glaucoma.
- These findings highlight the utility of Ca2+ imaging for glaucoma research.
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