Mouse Models of Retinal Degeneration in the MICRON Literature

About the MICRON Research Literature

These research pages organize published studies using MICRON imaging systems by animal species and the disease or condition investigated.

All publication counts and figures reflect the complete indexed research collection.

Explore related studies through the MICRON Research Hubs or search the complete publication collection in the reSEARCH portal.

Understanding Retinal Degeneration

Retinal degeneration names a group of conditions in which retinal cells are progressively lost, most often the photoreceptors and the retinal pigment epithelium they depend on.

The causes represented in this literature are varied:

• Inherited single-gene defects
• Light or chemical injury
• Processes associated with aging

What they share is the endpoint rather than the cause.

Retinal Degeneration in Experimental Research

The measurements that recur across them are correspondingly few:

• Photoreceptor loss and outer nuclear layer thinning read by cross-sectional imaging or histology
• A reduced electroretinographic response
• Where a study looks for it, a behavioral deficit

A model of one of these conditions reproduces the cell loss and its functional consequence; whether it also reproduces the human trigger, the time course or the spatial pattern of loss differs from model to model and is a property of the individual study rather than of the term.

Mouse Models of Retinal Degeneration

The mouse carries most of this work.

Transgenic and knockout lines allow a pathway to be removed or overexpressed, and cost, availability, short generation time and a large body of background data reinforce the choice.

A genetic manipulation constrains rather than isolates a mechanism: developmental compensation and pleiotropy remain possible.

Published MICRON Research: Retinal Degeneration in Mice

This page lists 280 papers from the MICRON literature, published 2011 to 2026, that study retinal degeneration in mice.

Of these publications:

• 277 studies used mice as the primary retinal degeneration disease model.
• 3 studies used healthy animals to assess pharmacokinetics, drug delivery, or tolerability.

Scope of the literature collection: Publication counts reflect studies identified and indexed in the MICRON research corpus. This collection is not intended to represent an exhaustive review of all published retinal degeneration research.

Which imaging and experimental techniques are used in these studies?

Technique counts are paper-level co-occurrences and do not necessarily indicate that a technique was applied to the focal species or focal disease model.

Capabilities and Limitations of Imaging Techniques

A summary of what each imaging technique listed above can measure, the information it provides, and its limitations in research applications.

Electroretinography

Records the retina's electrical response to light, giving component-sensitive information about outer- and inner-retinal function. It measures function directly, which no structural method does. Full-field ERG sums across the whole retina, so a small lesion can leave the trace unchanged; focal and multifocal variants trade signal amplitude for spatial resolution.

Optical Coherence Tomography

Optical coherence tomography provides high-resolution, cross-sectional images of ocular tissues in the living eye, allowing researchers to visualize structures at different depths. OCT is particularly useful for measuring tissue thickness, identifying structural abnormalities, and assessing the location and extent of tissue changes.

As a non-invasive imaging technique, OCT enables repeated measurements in the same eye over time, supporting longitudinal studies of disease progression and treatment response. Although OCT provides detailed structural information, it does not directly measure cellular activity or visual function. Tissue that appears structurally normal may still have functional abnormalities, making OCT a valuable companion to functional assessments such as electroretinography (ERG).

Topical Ophthalmic Drug Delivery

A compound applied as drops to the ocular surface. It is non-invasive and repeatable, so it supports frequent dosing without a procedure for each dose. What the route has to establish depends on the target: for an ocular-surface target, residence time and penetration into the surface tissue are the main barriers; for an intraocular anterior-segment target, the compound must cross ocular-surface and corneal or conjunctival barriers and reach an intraocular concentration sufficient for the experiment; for a posterior-segment target, additional ocular barriers separate the surface from the target and posterior-segment exposure is harder to establish.

Fundus Fluorescein Angiography

Fundus fluorescein angiography uses an injected fluorescent dye to visualize blood flow through the retinal and choroidal circulation. Sequential images show how vessels fill, identify areas of reduced or absent perfusion, and reveal dye leakage associated with vascular abnormalities.

This technique is particularly useful for evaluating vascular perfusion, blood-retinal barrier integrity, and abnormal vessel growth. Fluorescein angiography primarily shows dye distribution rather than the surrounding retinal tissue. It provides a two-dimensional (en face) view in which vessels at different depths may overlap. Cross-sectional and cellular structural details require other imaging methods, such as optical coherence tomography (OCT) or optical coherence tomography angiography (OCT-A). Vascular abnormalities that do not affect dye filling or produce leakage may also remain undetected.

Intravitreal Injection / Delivery

Injection into the vitreous places a substance directly into the vitreous at a known administered dose and chosen time, reducing but not eliminating systemic exposure. The injectate may be a therapeutic compound, cell preparation or viral vector, or an agent used to create the model, such as a toxin, vasoactive or excitotoxic compound, or infectious inoculum. The route bypasses surface-delivery barriers and provides direct access to the vitreous and posterior segment, but the concentration reached in a particular ocular tissue depends on distribution and clearance and is not fixed by the injected dose alone. It is invasive and discrete: each repeat dose or challenge requires another injection, and vehicle- or sham-injected controls can help separate effects of the injectate from effects of the procedure.

AAV-Mediated Ocular Gene Delivery

An adeno-associated viral vector delivers genetic material to ocular cells, and a single administration can support long-lived transgene expression. That persistence is useful for gene augmentation and sustained therapeutic-protein expression; AAV can also deliver gene-silencing or genome-editing cargo, where long-lived expression of the editing machinery may be unnecessary or undesirable. Capsid and route of delivery jointly determine which cells are reached, so different delivery routes and vector designs give different distributions.

CRISPR-Based Ocular Gene Editing

Uses a programmable genome-editing system to alter DNA at an endogenous locus rather than adding a separate replacement copy. Depending on the editor and design, it can disrupt, correct or install a sequence, either therapeutically or to create an experimental model. Once a genomic sequence change is established, the edit itself cannot be withdrawn like a dose; where the edit is present from conception, the resulting phenotype also reflects its effects throughout development. Off-target sequence changes are a separate question that structural imaging does not establish.

Optokinetic / Optomotor Response

Measures a reflexive head or eye movement tracking a moving pattern, giving a rapid, training-free behavioral estimate of spatial vision and contrast sensitivity in an animal that cannot report them. It is driven largely by reflex circuitry and reports on the visual pathway as a whole, so a deficit it detects still has to be localized by a structural or electrophysiological method, or separated from cortical processing by an operant task.

Optogenetics (Vision Restoration)

Optogenetic vision restoration introduces a light-sensitive protein into surviving retinal cells to restore or confer light responsiveness after native photoreceptor function has been lost. Depending on the strategy, the target may be residual cone cell bodies, bipolar cells or retinal ganglion cells. It is mutation-independent functional replacement rather than correction of the underlying disease gene. The sensitivity, spectral range, kinetics and amount of native retinal processing preserved depend on the opsin and target cell, and demonstrating light responsiveness is separate from demonstrating useful visual behavior.

Laser Photocoagulation Models

A laser lesion provokes a reproducible, quantifiable injury at a known time and place. Wavelength, power, duration, spot size, pulse mode, focus and lesion location together determine the injury produced, allowing laser exposure to be configured for different experimental endpoints. It is an induced injury, not the disease: it produces a lesion directly, bypassing the process that gives rise to comparable damage in patients.

Retinal Prosthesis / Electrode Array

A retinal prosthesis uses an implanted electrode array to deliver patterned electrical stimulation to surviving retinal neurons, with the aim of replacing visual input lost when photoreceptor function is severely impaired or absent. Arrays are commonly placed epiretinally, subretinally or suprachoroidally; placement strongly influences which retinal neurons are recruited and how much of the remaining retinal circuitry contributes to the response. Because the device supplies neural input rather than repairing the underlying degeneration, evaluation asks what the stimulation evokes: retinal or visual-pathway responses and visually guided behavior. Demonstrating that an array is implanted or evokes an electrical response is not the same as demonstrating useful functional vision.

Ocular Blast Injury

Experimental ocular blast models expose the eye, or in some paradigms the head with ocular outcomes measured, to a controlled overpressure wave at a known time. Peak pressure, waveform and impulse, exposure number, orientation and interval help determine the loading delivered to the eye. A blast wave can injure multiple ocular compartments, including anterior structures, retina and optic nerve, although the pattern and severity depend on the exposure paradigm and the animal. Eye-directed paradigms that shield the head and body are used to isolate primary blast effects on the eye; head-directed or less-confined paradigms may also involve central nervous-system and other traumatic-brain-injury mechanisms and should not be treated as equivalent. Because the exposure is known, interventions can be tested against it and sham exposures can help distinguish effects of the pressure wave from handling or the experimental procedure. Apparatus design, waveform, positioning and shielding materially affect the delivered exposure, so nominal pressure values or exposure counts should not be assumed directly comparable across laboratories or equivalent to human blast exposure without physical characterization.

Which MICRON systems and add-ons appear?

Which strains and genetic lines are used?

Which other species appear alongside?

What other conditions are recorded on the same papers?

The general term records an accepted mention of retinal degeneration without a subtype qualifier. It is not a roll-up: a paper carrying a subtype may or may not also carry the general term, depending on whether an unqualified mention of the family is also recorded elsewhere in the paper.

Which MICRON configurations appear in this work?

Configurations recorded in these papers, and the techniques recorded alongside them.

The papers

The table lists the 20 most recent papers in the cohort.

Browse all hubs at MICRON Research Hubs. The full corpus is searchable in the reSEARCH portal.