Research Applications for Striatech Products

The Optic Nerve, its Neurons and Diseases

Diseases of the optic nerve and retinal ganglion cells, including glaucoma and other optic neuropathies, cause progressive axon loss and irreversible blindness. This page highlights preclinical models of pressure‑dependent and pressure‑independent injury, neuroinflammation, glial and complement activation, aging‑related degeneration, and gene‑based therapies for optic nerve protection.
Research Chapter The Optic Nerve, its Neurons and Diseases

Diseases of the optic nerve and retinal ganglion cells, including glaucoma and other optic neuropathies, cause progressive axon loss and irreversible blindness. This page highlights preclinical models of pressure‑dependent and pressure‑independent injury, neuroinflammation, glial and complement activation, aging‑related degeneration, and gene‑based therapies for optic nerve protection.

16
Application Areas
6
FAQs answered
Part of Eye & Retinal Disease
Main Application Areas
Glaucoma
Optic Nerve Damage
Retinal Ganglion Cell Pathology
Additional Topics
Aging
Axon Degeneration
Blindness
Gene Therapy
Glial Suppression
Myopia
Neuroinflammation
Neurovascular Injury
Optic Nerve Regeneration
Optic Neuritis
Rare Disease
Retinal Degeneration
Retinal Ischemia-Reperfusion Injury
Introduction

What are Optic Nerve Diseases?

The optic nerve and its retinal ganglion cell (RGC) axons form the critical output pathway from the eye to the brain, and they are among the most vulnerable neurons to metabolic, vascular, inflammatory, and mechanical stress across the visual system. A broad spectrum of ocular and central nervous system disorders (including inherited and acquired optic neuropathies, optic neuritis, neurovascular and ischemic injuries, aging-related retinal degeneration, and rare genetic diseases) ultimately converge on progressive RGC loss and optic nerve damage that drive permanent visual field deficits and irreversible blindness. Within this wider family of optic nerve neurodegenerative diseases, glaucoma stands out as one of the most common conditions and a leading global cause of irreversible blindness, currently affecting tens of millions of people and projected to exceed 100 million cases as populations age.

Disease entities within this optic nerve and RGC neurodegeneration chapter span glaucoma, optic nerve damage and neuritis, retinal ganglion cell pathology, myopia-associated neurovascular changes, ischemia-reperfusion injury, and broader retinal degenerations, as well as aging-related axon degeneration, neuroinflammation, glial dysregulation, and rare inherited optic neuropathies. Their initiating insults differ, ranging from elevated intraocular pressure and mechanical strain at the optic nerve head to vascular occlusion, excitotoxicity, mitochondrial dysfunction, autoimmune demyelination, and pathogenic gene variants. Nevertheseless, these conditions frequently converge on shared downstream pathways: impaired axoplasmic transport, Wallerian-like axon self-destruction, glial-mediated neuroinflammation, disruption of neurovascular coupling, and chronic metabolic stress that together drive RGC soma loss and optic nerve degeneration. Experimental work in this area increasingly targets these convergent mechanisms, exploring neuroprotective strategies, modulation of microglia and astrocytes, glial suppression or reprogramming, and gene therapy approaches aimed at preserving or restoring axonal integrity and visual pathway function.

Across all these disease models, and regenerative or gene therapy studies, a central challenge is demonstrating that cellular and structural rescue translates into meaningful preservation or recovery of visual function. Behavioral assays based on optomotor and optokinetic responses in rodents, such as those implemented by Striatech’s OptoDrum system, provide objective, longitudinal measurements of visual acuity and contrast sensitivity that sensitively report the integrity of the retina–optic nerve–brain axis. By quantifying changes in these performance metrics over time, researchers can directly link aging, axon degeneration, glial and neuroinflammatory modulation, optic nerve regeneration, and gene therapy interventions to functional outcomes that mirror the visual field loss and blindness observed in human disease.

Vision: A Window into the brain 

Why Measure Visual Function in Optic Nerve Research?

For researchers whose primary interest is not clinical ophthalmology – including investigators studying CNS axon degeneration, axon regeneration, or neuroinflammation who use the optic nerve crush (ONC) model as a tractable in vivo platform – adding automated visual function measurement to an experimental workflow provides an orthogonal, functional endpoint that anatomical or histological readouts cannot supply on their own.

Anatomical evidence of axon regrowth distal to a crush site, or rescue of RGC soma counts, is necessary but not sufficient evidence of functional reconnection: a treatment that preserves RGC numbers or promotes axon extension into the superior colliculus, but fails to restore the optomotor reflex, has not achieved functional visual recovery.

The OptoDrum determines this non-invasively, at any time point, without interfering with the biology under study or the integrity of subsequent terminal analyses. Because the OMR is mediated by a subcortical reflex arc (retina → accessory optic system → nucleus of the optic tract → motor output), it reports directly on the integrity of the retino-recipient circuit rather than on cortical processing. For studies of axon regeneration and neuroprotection, this is precisely the circuit whose function needs to be demonstrated.

Also see: Maintaining and Restoring Vision.

Animal Models

Common Animal Models for Diseases Affecting the Optic Nerve

  • DBA/2J mice: A hereditary glaucoma model carrying mutations in Gpnmb and Tyrp1 that produce progressive iris disease and IOP elevation from approximately 6 months of age, followed by optic nerve degeneration and RGC loss. Visual acuity measured by OptoDrum declines in parallel with RGC loss, making this model well-suited to longitudinal natural-history studies and long-duration intervention trials in age-related glaucoma.
  • Microbead occlusion model (mice and rats): Intracameral injection of polystyrene or magnetic microbeads obstructs aqueous outflow through the trabecular meshwork, producing controllable IOP elevation followed by RGC degeneration. The magnitude and duration of IOP elevation, and the resulting functional visual decline, can be titrated by adjusting bead concentration and schedule, making the model adaptable to both acute and chronic experimental designs.
  • Laser-induced IOP elevation: Photocoagulation of the trabecular meshwork or episcleral veins creates outflow obstruction with reliable RGC loss and measurable OptoDrum acuity decline. Unilateral designs use the contralateral eye as an internal control, and the degree of IOP elevation and RGC loss can be modulated by adjusting laser parameters. Note that local retinal laser ablation alone does not lead to optomotor deficits.
  • Episcleral vein cauterisation (Morrison model, rats): Cauterisation of episcleral veins elevates IOP chronically in rats, producing a well-characterised model of moderate progressive glaucoma with gradual RGC degeneration and visual decline that parallels the clinical course of chronic open-angle glaucoma.
  • Soluble guanylate cyclase (sGC) deficiency mice: Genetic disruption of the principal NO-cGMP signalling axis in trabecular meshwork cells recapitulates glaucoma-like RGC degeneration and functional visual decline. OptoDrum was used to document this longitudinally across age, establishing sGC as a mechanistic driver of glaucomatous pathology. (Bossardet et al., 2026, Sci Rep.)
  • Optic nerve crush (ONC): A standardised surgical model in which the optic nerve is compressed briefly with calibrated forceps. ONC produces acute, near-complete RGC axon injury and rapid functional visual acuity loss detectable by OptoDrum within days to weeks. Because ONC does not involve IOP elevation, it is widely used as a pure axon injury model for studying neuroprotection, Wallerian degeneration, and axon regeneration – and serves as the primary in vivo platform for CNS axon biology groups for whom the optic nerve is a tractable CNS injury system.
  • Retinal ischemia-reperfusion injury (IRI): Transient acute IOP elevation via anterior chamber cannulation (typically 30 to 90 minutes), followed by reperfusion, creates oxidative stress, complement activation, and RGC death mimicking the ischemic component of acute angle-closure glaucoma attacks. OptoDrum detects functional visual decline within one to two weeks of injury. This model has been used to evaluate complement-pathway inhibitors (Zhao et al., 2025, Adv Sci (Weinh).) and necroptosis inhibitors (Kim et al., 2024, Cell Death Differ.)
  • NMDA-induced excitotoxicity: Intravitreal injection of N-methyl-D-aspartate selectively kills RGCs through glutamate-receptor-mediated excitotoxicity without affecting photoreceptors, enabling isolated study of RGC-specific cell death programmes and neuroprotectants targeting excitotoxic pathways.
Research Questions

How Can Striatech Tools support Your Study?

Select a question that matches your research objective to see which instruments are relevant, what challenge they address, and what the published evidence shows.
01
How Can I Measure Visual Acuity and Contrast Sensitivity Reliably in Preclinical Glaucoma Models?
Audience A - Vision-focused

Quick Answer

Striatech's OptoDrum measures spatial visual acuity (cycles per degree) and contrast sensitivity in awake, freely moving mice and rats via the automated optomotor reflex, without requiring animal training or anaesthesia. The assay takes less than 10 minutes per animal and can be performed repeatedly without affecting the animal's biology, making it ideal for longitudinal monitoring of glaucomatous visual decline. Both eyes can be assessed independently within a single session.

The challenge

Accurate, reproducible, and repeated measurement of visual function is the central methodological challenge in preclinical glaucoma research. The primary clinical endpoint of any therapeutic strategy – whether IOP-lowering, neuroprotective, or regenerative – is ultimately the preservation of visual function. Yet many preclinical studies rely exclusively on structural endpoints: RGC counts by immunohistochemistry, optic nerve axon density by electron microscopy, or retinal layer thickness by OCT. These endpoints are informative and necessary, but they are terminal or at minimum time-point-limited, they capture structure rather than function, and they cannot demonstrate that structural preservation translates into a functioning retino-cortical circuit. Electrophysiological endpoints such as ERG and VEP provide functional information but typically require anaesthesia (which affects retinal responses), specialised equipment and technical expertise, and are logistically demanding for high-throughput longitudinal applications.

The optomotor reflex offers a fundamentally different approach: it is a reflexive, subcortical behaviour that does not require the animal to have learned any task, that can be measured repeatedly in the same animal across weeks or months, and that directly reports on the integrity of the retino-brainstem pathway.

How Striatech products help

OptoDrum
Automatically measures photopic spatial visual acuity (cycles per degree) and contrast sensitivity threshold via the optomotor reflex in awake, freely moving mice and rats. Enables daily or weekly longitudinal profiling across the full course of glaucomatous disease or experimental intervention.
AcuiSee
Measures visual acuity and contrast sensitivity via an operant, forced-choice paradigm requiring cortical visual processing and active decision-making. Complements OptoDrum for studies that also wish to assess suprathreshold visual perception or cognitive dimensions of visual function (for example, in aging or neurodegeneration co-morbidity contexts). Note that AcuiSee requires a training phase of 10 to 14 days.
Non-aversive Animal Platform
Allows animals to voluntarily enter the OptoDrum testing environment from their home cage via a tunnel-lid design. Reduces handling stress, which can introduce variability in the optomotor response; particularly relevant for aged DBA/2J mice or post-surgical animals who may be difficult to handle conventionally.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Mickevičius et al (2025) Exp Eye Res.
    In a comprehensive characterisation of a preclinical glaucoma model, the authors used OptoDrum to establish the time course over which structural RGC changes – cell death, axon damage, and optic nerve histopathology – map onto functional visual acuity decline. This study provides the benchmark correlation between structural glaucomatous endpoints and the OptoDrum readout, confirming that spatial acuity loss is a reliable functional correlate of progressive RGC neurodegeneration.
02
How Does Neuroinflammation Drive Retinal Ganglion Cell Loss in Glaucoma, and Can Targeting Inflammatory Pathways Preserve Visual Function?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Neuroinflammation – mediated by TNF-α, complement cascade activation, and reactive microglial and glial responses – is a central driver of RGC death in both acute and chronic glaucoma. Studies, using the OptoDrum, show that targeting these inflammatory pathways pharmacologically, or suppressing glial activation, preserves measurable visual acuity in multiple preclinical glaucoma models, establishing the anti-inflammatory approach as a validated functional neuroprotective strategy.

The challenge

Neuroinflammation in glaucoma is not a secondary bystander response but an active amplifier of primary pressure-dependent and pressure-independent injury. Activated microglia produce TNF-α, which binds TNFR1 on RGCs and drives apoptosis via the extrinsic death pathway; simultaneously, complement proteins C1q, C3, and their receptor C3aR are upregulated at the optic nerve head and inner retina, promoting synaptic elimination, membrane-attack-complex formation, and phagocytic RGC clearance. Reactive astrogliosis further compromises the metabolic support provided to RGC axons at the lamina cribrosa. Each of these components represents a potential therapeutic target, but demonstrating that any intervention translates from a reduction in inflammatory markers or histological RGC rescue to a genuine improvement in functional vision has historically been difficult without a reliable, non-invasive functional readout.

Also see: Neuroinflammation and Autoimmune CNS Disease and Retinal Degeneration.

How Striatech products help

OptoDrum
Provides the functional confirmation endpoint for anti-neuroinflammatory interventions in glaucoma. Measures spatial acuity and contrast sensitivity longitudinally, enabling researchers to determine whether a reduction in TNF-α signalling, complement activation, or microglial hyperactivation achieved at the molecular level translates to preserved circuit-level visual performance.
AcuiSee
Provides a cortically mediated, operant visual acuity endpoint for neuroinflammation-driven RGC loss in glaucoma. Confirms whether anti-inflammatory interventions preserve learned visual discrimination and suprathreshold cortical visual processing, complementing the subcortical reflex readout from OptoDrum.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Li et al (2025) Neurosci Bull.
    This study demonstrated that TNF-α-mediated neuroinflammation drives optic nerve damage and RGC death in a glaucoma model, with OptoDrum confirming that TNF-α-induced structural loss translates to quantifiable functional visual acuity decline. The study provides direct evidence for the TNF-α axis as a driver of measurable visual impairment in glaucoma, not merely a marker of histological damage.
  • Zhao et al (2025) Invest Ophthalmol Vis Sci.
    This study characterised complement C3/C3aR signalling as a neuroinflammatory cascade driving RGC dysfunction following retinal ischemia-reperfusion injury – a model relevant to acute IOP spike-induced RGC damage in angle-closure glaucoma. OptoDrum confirmed functional visual acuity loss resulting from complement-mediated injury. The study adds the complement pathway as a second mechanistic neuroinflammation target alongside TNF-α.
  • Zeng et al (2022) Biomolecules
    This study demonstrated that systemic treatment with pioglitazone, a PPAR-γ agonist, reduces neuroinflammation in a glaucoma model and – critically – preserves visual acuity as measured by OptoDrum, confirming that broad anti-inflammatory pharmacotherapy translates from reduced inflammatory histology to functional visual neuroprotection.
03
Do Neuroprotective Compounds and Gene Therapies Preserve or Restore Visual Function in Glaucoma Models?
Audience A - Vision-focused

Quick Answer

Multiple neuroprotective strategies – including SARM1-pathway targeting, RNA-based gene editing, nitric oxide-donating pharmacology, and novel drug delivery systems – have been shown to preserve OptoDrum-measured visual acuity in preclinical glaucoma models, demonstrating that structural RGC protection translates to measurable circuit-level functional benefit. OptoDrum provides the non-invasive functional endpoint that validates each intervention at the level that matters for clinical translation.

The challenge

Reduction of intra-ocular pressure (IOP) is the most common first-line treatment strategy in glaucoma, but IOP lowering alone does not halt glaucoma progression in a substantial proportion of patients. There is a clear unmet need for IOP-independent neuroprotective strategies. Numerous candidate approaches have been advanced preclinically – targeting programmed cell death pathways, inflammatory mediators, metabolic support, and epigenetic dysregulation – but demonstrating that any of these translates from preserved RGC counts to genuinely preserved or restored visual function is the critical translational step. The structural rescue of RGCs that are subsequently non-functional, or the anatomical regrowth of axons that fail to establish synaptic contacts, does not constitute a meaningful preclinical outcome for therapeutic development. OptoDrum addresses this gap by providing a sensitive, non-invasive, and repeatable functional endpoint throughout an intervention study, enabling researchers to track the time course of protection, determine whether protection is sustained, and identify the optimal therapeutic window.

Also see: Gene Therapy and Maintaining and Restoring Vision.

How Striatech products help

OptoDrum
Provides the longitudinal functional endpoint for neuroprotective and gene therapy efficacy testing in glaucoma. Measures spatial acuity and contrast sensitivity non-invasively at any time point, enabling determination of the onset, magnitude, and durability of functional protection or restoration. Requires no animal training and can be performed on as many time points as the study demands without confounding subsequent terminal analyses.
AcuiSee
Provides a cortically mediated, operant visual acuity endpoint for neuroprotection and gene therapy studies in glaucoma. Confirms whether interventions that preserve RGCs and optic nerve integrity also maintain cortical visual discrimination – a higher-order functional confirmation the subcortical optomotor reflex does not capture.
Non-aversive Animal Platform
Reduces handling stress for post-surgical or debilitated animals, ensuring reliable optomotor responses from animals that may be compromised following intraocular injection or optic nerve surgery and that would otherwise produce unreliable data.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Zhao et al (2025) Adv Sci (Weinh).
    This study developed a high-fidelity RNA-targeting CRISPR-Cas system and demonstrated in a preclinical glaucoma model that gene-editing-mediated silencing of pathogenic targets preserves both RGC survival and OptoDrum-measured visual acuity.
  • Zeng et al (2024) Acta Neuropathol Commun.
    Genetic deletion of SARM1, the central NADase of the Wallerian axon self-destruction programme, reduced RGC death in a glaucoma model. Critically, OptoDrum confirmed that this structural axon and soma protection translated to preserved spatial visual acuity, establishing SARM1 as a therapeutic target whose functional benefit is demonstrable at the circuit level. SARM1 inhibition is an active area of neurodegeneration drug development.
  • Pan et al (2025) J Med Chem.
    This medicinal chemistry study identified novel nitric oxide-donating compounds with dual mechanisms in glaucoma – IOP reduction and direct RGC neuroprotection. OptoDrum confirmed that these pharmacological effects preserved visual acuity, providing the translational functional validation required for the candidate compound programme.
  • Yang et al (2022) J. Med. Chem.
    An earlier study from the same NO-donor programme, providing historical depth for the pharmacological approach and confirming OptoDrum sensitivity to the functional effects of nitric oxide-based glaucoma pharmacology.
  • Lin et al (2022) Biomater. Sci.
    This biomaterials study introduced a novel glaucoma mouse model: intraocular injection of an in situ-crosslinked hydrogel mediated reliable pressure increase, resulting in reduced visual acuity as assessed by OptoDrum, illustrating that the functional readout is applicable not only to molecular target studies but also to delivery system validation and model characterization.
04
How Do I Track Glaucoma Progression Longitudinally and Identify the Optimal Therapeutic Window?
Audience A - Vision-focused

Quick Answer

OptoDrum enables weekly or even daily longitudinal measurement of spatial visual acuity in awake animals throughout the full course of experimental glaucoma, from baseline through disease progression to endpoint. This non-invasive, repeated-measures approach allows precise identification of the onset of functional visual decline – and therefore of the therapeutic window – within individual animals, removing the need to sacrifice separate cohorts at multiple time points to reconstruct a progression curve.

The challenge

Identifying the optimal therapeutic window – the period during which RGCs are injured but not yet irreversibly lost, and therefore still rescuable – is one of the most practically important and methodologically demanding aspects of preclinical glaucoma research.

Traditional approaches infer progression from structural data (RGC counts, nerve fibre layer thickness) collected in separate cohorts at pre-specified time points, which are expensive in animal numbers, confound between-subject variability with temporal progression, and fail to capture within-individual inflection points in functional decline.

A functional biomarker that can be measured repeatedly in the same animal – as OptoDrum provides – transforms the experimental design: instead of inferring population-level curves from cross-sectional cohorts, the researcher can establish individual trajectories and identify the precise moment of functional onset for each animal, then stratify intervention timing accordingly. This precision is particularly important in aging-disease interactions (such as age-dependent glaucoma in DBA/2J mice) where the onset of IOP elevation and functional decline is variable between individuals. For researchers studying rare or inherited glaucoma subtypes, the model selection question – which genetic background provides the most relevant visual phenotype – is a prerequisite for longitudinal programme design, and OptoDrum provides the visual phenotyping needed to make that comparison.

Also see: Rare and Inherited CNS and Eye Disorders, Myopia, Refractive Development and Eye Growth, Myopia and Blindness.

How Striatech products help

OptoDrum
Measures spatial acuity and contrast sensitivity longitudinally at any frequency (weekly, biweekly, or daily in acute models). Provides a within-subject functional timeline that enables precise identification of functional decline onset, plateau, and response to intervention. No animal training or anaesthesia; approximately 4 minutes per animal; compatible with concurrent structural assessments at the same time points.
AcuiSee
Provides a cortically mediated, operant visual acuity endpoint for longitudinal tracking of glaucoma progression. May reveal progressive impairment in learned visual discrimination as RGC loss advances, complementing the subcortical reflex trajectory from OptoDrum.
Non-aversive Animal Platform
Ensures consistent optomotor responses across repeated testing sessions for aged, handled-sensitive, or chronically diseased animals – reducing the test-to-test variability that can obscure the early stages of functional decline when the therapeutic window is most critical to identify.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Baya Mdzomba et al (2020) Cell Death Dis.
    Journal Club →
    This study's main readout was behavioral visual function in response to an excitotoxic NMDA insult, showing baseline function, visual acuity decline and recovery, and the effects of treatment. This is a prime example of non-invasive disease progression monitoring with the OptoDrum.
  • Bossardet et al (2026) Sci Rep.
    This study assessed functional visual acuity in two age groups using OptoDrum in sGC-deficient mice, documenting the natural history of progressive glaucoma-like visual decline in a genetically defined model. This study demonstrated that this specific genetic model caused functional decline specifically in female individuals.
  • Kuchtey et al (2024) Am J Ophthalmol.
    This systematic evaluation of mouse models for rare and inherited glaucoma used OptoDrum to phenotype the visual deficit severity across candidate genetic backgrounds, providing the functional characterisation needed to select the most appropriate model for a longitudinal therapeutic programme. Establishing the baseline phenotype and rate of decline is a prerequisite for designing an appropriately powered intervention study with defined therapeutic windows.
  • Insignares et al (2025) Int J Mol Sci.
    This study characterised progressive ocular axial elongation and secondary optic nerve damage in Loxl1−/− mice, using OptoDrum to document their functional visual abilities. This mouse model did not show functional optomotor decline, despite other ganglion cell related deficits - important baseline information about what can and cannot be assessed through behavioral visual readouts.
05
How Does Aging Interact with Glaucomatous Neurodegeneration, and Can Visual Function Serve as a Readout of Age-Glaucoma Pathology?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Aging amplifies virtually every component of glaucomatous neurodegeneration – increasing basal neuroinflammation, impairing RGC metabolic resilience, reducing the capacity for axon repair, and accelerating the epigenetic dysregulation associated with RGC loss. Studies demonstrate that age-associated visual decline is measurable and partially reversible through epigenetic reprogramming gene therapy.

The challenge

Age is the single largest non-modifiable risk factor for glaucoma: the prevalence of the disease rises steeply after 60 years of age, and normal aging itself reduces RGC density, degrades axon transport efficiency, and shifts the microglial phenotype toward a proinflammatory state that amplifies pressure-dependent injury. Preclinical researchers working with aging glaucoma models therefore face compounded variability: the degree of IOP elevation, the rate of RGC loss, and the time course of functional visual decline all vary between individual animals in an age-dependent way that is difficult to control by group assignment alone. A functional biomarker that tracks each animal individually – as the OptoDrum provides – is therefore particularly valuable in the aging-glaucoma intersection, where within-group variance is high and individual inflection points matter for therapeutic window determination. Beyond tracking decline, an important emerging question is whether age-related epigenetic changes that reduce RGC resilience can be pharmacologically reversed. The OSK gene therapy programme (Karg et al., 2023, Cell Reprogram.) has demonstrated proof-of-concept for this reversal, with optomotor readouts as the primary endpoint for functional vision recovery.

Also see: Systemic Aging and CNS Decline, Aging and Maintaining and Restoring Vision.

How Striatech products help

OptoDrum
Tracks age-related visual acuity and contrast sensitivity decline longitudinally in the same animal across weeks and months. In aging models (such as DBA/2J mice or sGC-deficient aging cohorts), within-animal tracking allows precise determination of when age-related functional decline begins in each individual, avoiding the misclassification that arises from cross-sectional sampling of an inherently variable aging population.
AcuiSee
In aging studies where cortical processing and visual cognitive function are also of interest – for example, in studies examining both retinal and cortical aspects of age-related visual decline – AcuiSee's operant paradigm complements the OptoDrum's subcortical OMR endpoint by assessing the suprathreshold, decision-making dimension of visual perception.
Non-aversive Animal Platform
Particularly important for aged animals, which are more sensitive to handling stress and more likely to produce inconsistent optomotor responses under conventional restraint. The tunnel-lid design allows voluntary entry from the home cage, reducing the confounding effect of stress-induced behavioural suppression in aged cohorts.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Karg et al (2023) Cell Reprogram.
    Journal Club →
    Sustained recovery of visual acuity was demonstrated in an aging glaucoma mouse model following AAV-mediated delivery of OSK (Oct4/Sox2/Klf4) epigenetic reprogramming factors. OptoDrum served as the primary functional endpoint, showing that acuity lost to combined aging and glaucomatous damage was measurably and durably restored following OSK treatment. This study represents the most direct available evidence that OptoDrum can detect functional vision recovery – not only decline – in an age-glaucoma model, and it provides the benchmark functional outcome for the epigenetic reprogramming approach.
  • Hollingsworth et al (2022) Front. Pharmacol.
    Journal Club →
    This study examined chronic proinflammatory conditions in an aging mouse model and documented progressive visual acuity decline using OptoDrum.
06
Can Optic Nerve Injury and Ischemia-Reperfusion Models Inform Neuroprotective and Regenerative Strategies Relevant to Glaucoma?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Optic nerve crush (ONC), retinal ischemia-reperfusion injury (IRI), and acute intra-ocular pressure (IOP) elevation models provide well-controlled, rapid-onset injury systems that are widely used to evaluate neuroprotective compounds, axon-regenerative strategies, and mechanistic targets relevant to glaucoma. Studies, using the OptoDrum, in these models have identified RIP1 kinase inhibition, zinc transporter deletion, erythropoietin administration, and dopaminergic circuit modulation as candidates with demonstrated functional visual benefit. Critically, OptoDrum provides the functional validation that structural neuroprotection has translated to circuit-level visual preservation.

The challenge

ONC and IRI models occupy an important strategic position in preclinical glaucoma research: they produce rapid, reproducible, and quantifiable injury to the optic nerve and RGC population within a compressed time frame, enabling high-throughput evaluation of candidate neuroprotective and regenerative interventions before committing to the longer and more resource-intensive chronic glaucoma models.

A central challenge in interpreting data from these acute models is demonstrating that the structural outcomes most commonly reported – RGC survival counts, axon density measurements, or anterograde axon tracer results – translate to genuine functional visual improvement. Anatomical evidence of axon regrowth following a regeneration-promoting intervention, for example, does not confirm that the regenerated axons have re-established functional synaptic contacts with their targets in the brain.

OptoDrum addresses this directly: it measures the functional optomotor output of the retino-brainstem circuit and can distinguish animals with genuine visual circuit recovery from those with structural rescue that has not been functionally integrated. For researchers not primarily working in ophthalmology, visual function measurement with OptoDrum adds a validated functional endpoint to what would otherwise be a purely anatomical or molecular experimental output.

Also see: Trauma and Acute Injury, Optic Nerve Damage, Axon Degeneration, Optic Nerve Regeneration, Retinal Ischemia-Reperfusion Injury and Optic Neuritis.

For inherited forms of optic neuropathy – such as Wolfram syndrome optic atrophy – in which metabolic failure and neuroinflammation drive progressive optic nerve degeneration through mechanisms overlapping with those described here, see: Rare and Inherited CNS and Eye Disorders.

How Striatech products help

OptoDrum
Measures functional visual acuity and contrast sensitivity at any time point following ONC, IRI, or acute IOP elevation, providing the critical functional endpoint that confirms whether structural neuroprotection or axon regeneration has translated to circuit-level visual recovery. Non-invasive, requires no training, takes less than 10 minutes per animal; can be performed as frequently as needed without interfering with concurrent molecular or histological analyses.
AcuiSee
Provides a cortically mediated, operant visual acuity endpoint for optic nerve injury and ischaemia-reperfusion studies. Assesses whether neuroprotective or regenerative interventions restore learned visual discrimination, confirming cortical visual processing recovery beyond subcortical reflex improvement.
Non-aversive Animal Platform
Reduces handling stress for post-surgical animals recovering from ONC or IRI procedures, ensuring consistent optomotor responses in the early post-injury period when animals may be physically compromised and in which data quality is most critical for identifying the temporal profile of functional decline and recovery.
DarkAdapt
ScotopicKit
When scotopic (rod-mediated) visual function is also of interest – for example, in ONC studies examining whether rod pathways are differentially spared relative to cone pathways, or in inherited optic neuropathy models where rod function may decline earlier – DarkAdapt provides the light-tight housing needed to dark-adapt animals prior to scotopic OMR testing with the OptoDrum ScotopicKit extension.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Kim et al (2024) Cell Death Differ.
    Journal Club →
    Feature →
    RIP1 kinase inhibition protected RGCs from necroptotic death and attenuated neurovascular injury in a retinal ischemia-reperfusion model. OptoDrum confirmed that this structural neuroprotection translated to preserved visual acuity, establishing RIP1 kinase as a validated functional neuroprotective target in an acute glaucoma-relevant injury setting.
  • Liu et al (2023) Neural Regen Res.
    Selective deletion of a zinc transporter reduced axon degeneration and promoted optic nerve regeneration following ONC, with OptoDrum confirming that structural improvements in axon integrity corresponded to improved functional visual acuity. This study identifies zinc transporter modulation as a candidate neuroprotective-regenerative target with demonstrated functional benefit in the ONC model.
  • Eghbali et al (2023) Cell J.
    Erythropoietin protected RGCs from degeneration following optic nerve injury partly by suppressing reactive glial activation. OptoDrum confirmed that the structural neuroprotection and anti-neuroinflammatory effects of EPO translated to preserved visual acuity, supporting EPO's translational potential for optic neuropathies with a glial-mediated inflammatory component.
  • Li et al (2023) Life Sci. Alliance
    Feature →
    Vitamin C (ascorbic acid) provided antioxidant neuroprotection for RGCs in an optic nerve damage model, with OptoDrum confirming that antioxidant-mediated structural RGC protection translated to preserved visual acuity.
  • Rossi et al (2023) Elife
    MCT1-dependent metabolic failure in oligodendrocytes was shown to drive secondary neuroinflammation and progressive optic nerve degeneration in a Wolfram syndrome model, with OptoDrum measuring progressive visual acuity loss as the functional readout of optic neuropathy.
Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum ScotopicKit AcuiSee Photorefractor Keratometer DarkAdapt Non-aversive platform
Measuring visual acuity and contrast sensitivity Yes Yes Yes
Neuroinflammation and RGC loss Yes Yes
Neuroprotection and gene therapy Yes Yes Yes
Longitudinal tracking Yes Yes Yes
Aging and glaucoma Yes Yes Yes
ONC and acute injury models Yes Yes* Yes Yes* Yes
* ScotopicKit and DarkAdapt are relevant for ONC and acute injury models when scotopic (rod-mediated) visual function is also a study endpoint.
Measurement Modalities

Measuring Functional Visual Outcomes in The Optic Nerve, its Neurons and Diseases: How Do Available Methods Compare?

Glaucoma preclinical research uses a range of modalities to assess the consequences of RGC degeneration and the efficacy of interventions. The table below compares the principal options across dimensions most relevant to research design decisions. Striatech's tools are most valuable when combined with structural and electrophysiological endpoints, not as replacements for them.
Modality What It Measures Invasiveness Repeatability in the same animal Training required Automation 3Rs relevance
OptoDrum (Striatech) Spatial visual acuity and contrast sensitivity via optomotor reflex (subcortical) Non-invasive; no anaesthesia High; can be performed daily None Fully automated Refinement (no restraint, no anaesthesia); enables Reduction (replaces some terminal cohorts)
AcuiSee (Striatech) Visual acuity and contrast sensitivity via operant forced-choice (cortical) Non-invasive; food restriction required High after training phase 10 to 14 days Automated after training Refinement; provides psychophysical cortical endpoint complementary to OMR
Scotopic ERG Rod and cone photoreceptor function; inner retinal function (b-wave, pSTR) Moderate; typically requires anaesthesia and pupil dilation Moderate; anaesthesia imposes practical limits on frequency Operator skill required Semi-automated Moderate; anaesthesia constitutes a physiological perturbation
Pattern ERG (PERG) RGC-specific electrophysiological response to patterned stimuli Moderate; requires anaesthesia and corneal electrode placement Moderate Operator skill required Semi-automated Moderate; more specific to RGC function than flash ERG; complements OMR
Visual Evoked Potential (VEP) Cortical response to visual stimulation; assesses the full retino-cortical pathway Invasive; requires surgical electrode implantation in most protocols Low to moderate depending on electrode implant High; surgical implantation and signal processing expertise Low Lower 3Rs score due to surgical invasiveness; cortical endpoint complements OMR
Optical coherence tomography (OCT) Retinal layer thicknesses including RNFL and GCL; structural endpoint only Low to moderate; typically requires anaesthesia or restraint for rodents High Operator skill required for image acquisition and segmentation Semi-automated segmentation Structural endpoint; does not measure functional vision; complements OMR
Histological RGC counting RGC soma and axon density at a single time point; structural endpoint only Terminal None (terminal) Moderate histological expertise Partially automated (image analysis) Terminal; limits the number of time points per animal; replaced by repeated OMR for longitudinal studies
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Publications on The Optic Nerve, its Neurons and Diseases

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Journal Clubs related to The Optic Nerve, its Neurons and Diseases

Featured image for “Journal Club: RIP1 Inhibition Protects Retinal Ganglion Cells in Preclinical Glaucoma Models”
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Wednesday, 18 Jun 2025

Journal Club: RIP1 Inhibition Protects Retinal Ganglion Cells in Preclinical Glaucoma Models

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Bo Kyoung Kim, Ph.D. - Roche Pharma Research & Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd.
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This Journal Club features innovative research by Kim et al., who revealed that inhibiting RIP1 kinase protects retinal ganglion cells in preclinical glaucoma models. Their work demonstrates that targeting necroptosis and inflammation can prevent cell loss and functional decline, directly linking genetic risk to inflammatory degeneration and highlighting RIP1 as a promising therapeutic target for neuroprotection in glaucoma.
Featured image for “Journal Club: Aging and Injured Retinal Ganglion Cells Can Be Rejuvenated by Epigenetic Reprogramming”
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Thursday, 27 Feb 2025

Journal Club: Aging and Injured Retinal Ganglion Cells Can Be Rejuvenated by Epigenetic Reprogramming

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Bruce R. Ksander, Ph.D. - Schepens Eye Institute of Mass Eye & Ear, Harvard Medical School, Department of Ophthalmology
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This Journal Club highlights groundbreaking work by Harvard Medical School scientist Bruce R. Ksander and his team. They were able to reverse aging in retinal ganglion cells, improving visual function after injury or in disease.
Featured image for “Webinar: AcuiSee – Rodent Visual Acuity Using Behavioral Conditioning”
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Wednesday, 17 Nov 2021

Webinar: AcuiSee – Rodent Visual Acuity Using Behavioral Conditioning

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Dr. Jeffrey A Jamison - Experimentica Ltd.
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In this Webinar, Dr. Jeff Jamison will talk about “AcuiSee”, with which one can measure rodent vision based on an operant conditioning paradigm. Jeff is the developer of AcuiSee, and he now works as Director of In-Vivo Pharmacology at Experimentica.
Featured image for “Journal Club: The role of Nogo-A in visual deficits induced by retinal injury.”
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Thursday, 28 Jan 2021

Journal Club: The role of Nogo-A in visual deficits induced by retinal injury.

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Julius Baya Mdzomba, PhD - Université Laval
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Nogo-A is an inhibitor of neurite and axon growth that can limit CNS repair after injury. Neutralizing Nogo-A can aid recovery, including recovery of visual function after retinal injury. Baya Mdzomba and colleagues used OptoDrum to show improved optomotor visual function after Nogo-A neutralization in an NMDA-induced excitotoxic retinal-injury model.
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Related application areas, neighbouring research chapters, and the questions researchers ask most.

Research Chapter The Optic Nerve, its Neurons and Diseases

Diseases of the optic nerve and retinal ganglion cells, including glaucoma and other optic neuropathies, cause progressive axon loss and irreversible blindness. This page highlights preclinical models of pressure‑dependent and pressure‑independent injury, neuroinflammation, glial and complement activation, aging‑related degeneration, and gene‑based therapies for optic nerve protection.

16
Application Areas
6
FAQs answered
Part of Eye & Retinal Disease
Main Application Areas
Glaucoma
Optic Nerve Damage
Retinal Ganglion Cell Pathology
Additional Topics
Aging
Axon Degeneration
Blindness
Gene Therapy
Glial Suppression
Myopia
Neuroinflammation
Neurovascular Injury
Optic Nerve Regeneration
Optic Neuritis
Rare Disease
Retinal Degeneration
Retinal Ischemia-Reperfusion Injury

This page has been generated in part with support of AI. Before publication it has been reviewed by a Striatech editor.

Last updated: 3 August 2026