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Glaucoma: Overview

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...

Open Angle Glaucoma: Treatment

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...

Angle Closure Glaucoma: Treatment

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...

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Related Experiment Video

Updated: Jun 16, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

Calpain activation in experimental glaucoma.

Wei Huang¹, John Fileta, Ian Rawe

¹Howe Laboratory of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA 02114, USA.

Investigative Ophthalmology & Visual Science

|January 29, 2010

Summary

This summary is machine-generated.

Calpain activation occurs in experimental glaucoma, contributing to retinal ganglion cell loss. This study provides evidence linking elevated intraocular pressure to neurodegeneration via calpain-mediated pathways.

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Area of Science:

Neuroscience
Ophthalmology

Background:

Glaucoma is a neurodegenerative disease characterized by elevated intraocular pressure (IOP) and progressive retinal ganglion cell (RGC) loss.
Calcium dysregulation is implicated in RGC death, with calpain activation a potential mechanism in neurodegeneration.

Purpose of the Study:

To investigate the hypothesis that calpain activation contributes to RGC loss in glaucoma.
To explore the role of calcium-induced calpain activity in the pathogenesis of experimental glaucoma.

Main Methods:

Utilized a rat model of experimental glaucoma with elevated IOP.
Employed immunoblot analysis, immunoprecipitation, MALDI-ProTOF/MS, and immunohistochemistry to detect calpain activation and substrate cleavage.

Main Results:

Detected an active 55-kDa form of calpain in glaucomatous rat retinas.
Demonstrated cleavage of calpain substrates spectrin and calcineurin exclusively in eyes with elevated IOP.
Confirmed calpain-mediated spectrin and calcineurin cleavage in RGCs under elevated IOP conditions.

Conclusions:

Provided four lines of evidence supporting calpain activation in experimental glaucoma.
These findings support the role of calpain in the pathological events leading to RGC death in glaucoma.