Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Rafael Lani-Louzada; Carla Andreia Abreu; Victor G. Ara&#250;jo; Mariana S. Dias; Hilda Petrs-Silva; Rafael Linden

doi:10.3791/63442

Cautérisation complète du plexus vasculaire limbique pour le glaucome induit chirurgicalement che...

JoVE Journal
Neuroscience

A subscription to JoVE is required to view this content. Sign in or start your free trial.

JoVE Journal Neuroscience

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Cautérisation complète du plexus vasculaire limbique pour le glaucome induit chirurgicalement chez les rongeurs

Full Text

1,925 Views

10:10 min

February 15, 2022

DOI: 10.3791/63442-v

Rafael Lani-Louzada¹, Carla Andreia Abreu¹, Victor G. Araújo¹, Mariana S. Dias¹, Hilda Petrs-Silva¹, Rafael Linden¹

¹Instituto de Biofísica Carlos Chagas Filho,Universidade Federal do Rio de Janeiro

Please note that some of the translations on this page are AI generated. Click here for the English version.

Overview

This study presents a novel model of glaucomatous neurodegeneration induced by 360° thermic cauterization of the limbal vascular plexus, leading to subacute ocular hypertension. The model allows for the investigation of glaucoma pathophysiology and utilizes a non-invasive, low-cost methodology for in vivo functional analysis.

Key Study Components

Area of Science

Neuroscience
Ophthalmology
Neurodegeneration

Background

Glaucoma is a significant cause of optic nerve degeneration and vision loss.
Understanding the underlying mechanisms can aid in developing therapeutic strategies.
The model is designed to study progressive neurodegeneration in the retina and optic nerve.
The method is reproducible and requires fewer animals, enhancing experimental efficiency.

Purpose of Study

To establish a robust model for studying glaucoma.
To investigate the effects of ocular hypertension on retinal and optic nerve integrity.
To enable analyses of neuronal responses using various assessment techniques.

Methods Used

The model involves 360° cauterization of the limbal vasculature to induce elevated intraocular pressure.
Rats are used as the biological model, and surgery is performed to induce ocular hypertension.
Intraocular pressure measurements and optomotor response evaluations are key methodological steps.
Histological assessments of retinal ganglion cells are performed post-surgery.
Electrophysiological recordings, including pattern electroretinogram, are conducted to evaluate retinal function.

Main Results

The study successfully demonstrates retinal and optic nerve degeneration in response to induced ocular hypertension.
Key findings include alterations in intraocular pressure and subsequent changes in visual function as evidenced by optomotor responses.
Histological analysis confirms the loss of retinal ganglion cells, demonstrating the model's validity.
Electrophysiological data show significant impairments indicative of glaucomatous damage.

Conclusions

This novel model provides a valuable platform for studying the pathophysiology of glaucoma.
The findings offer insights into neurodegenerative processes relevant not only to glaucoma but potentially to other neural disorders.
The study establishes a foundation for future research into treatment and intervention strategies in ocular and neurodegenerative diseases.

Frequently Asked Questions

What are the advantages of this glaucomatous model?

The model allows for easy learning, is non-invasive, low-cost, and highly reproducible, providing efficient experimental designs.

How is ocular hypertension induced in the model?

Ocular hypertension is induced by cauterizing the limbal vasculature around 360 degrees of the cornea.

What types of assessments are performed in this study?

The study includes intraocular pressure measurements, optomotor responses, and histological evaluations of retinal ganglion cells.

How can this model be adapted for other research?

The methodology can be modified for different durations and types of interventions, allowing investigation into various neurodegenerative conditions.

What are the key limitations of this model?

Though reproducible, the model's findings may not fully translate to human glaucoma due to species differences in ocular anatomy and disease progression.

What implications do the findings have for understanding neuronal mechanisms?

The findings elucidate retinal and optic nerve degeneration processes, potentially informing research into broader neurodegenerative mechanisms.

L’objectif de ce protocole est de caractériser un nouveau modèle de neurodégénérescence glaucomateuse basé sur une cautérisation thermique à 360° du plexus vasculaire limbique, induisant une hypertension oculaire subaiguë.

Nous avons développé une méthode simple pour induire une dégénérescence robuste et progressive du glaucome basée sur une élévation temporaire de la pression intraoculaire. Il s’agit d’une occasion unique d’étudier les points clés de la physiopathologie du glaucome. Il s’agit d’un modèle facile à apprendre, non invasif, peu coûteux et hautement reproductible qui permet une analyse de la fonction in vivo et des plans expérimentaux à court terme utilisant un nombre réduit d’animaux pour chaque expérience.

La rétine et le nerf optique sont des parties évaluables du système nerveux central, de sorte que la modélisation de la déficience progressive de ces structures peut fournir des informations précieuses sur d’autres troubles neurodégénératifs. Pour mesurer la pression intraoculaire initiale, ou PIO, des yeux témoins expérimentaux et controlatéraux, placez le rat anesthésié dans une position de décubitus ventral sur la paillasse, de sorte que la surface cornéenne soit facilement accessible à l’extrémité du tonomètre. Positionnez la pointe du tonomètre de manière à ce qu’elle touche légèrement la zone cornéenne centrale perpendiculairement.

View the full transcript and gain access to thousands of scientific videos