Search Results (213)

Objective: To investigate the neuroprotective effects of a Rho-associated kinase (ROCK) inhibitor on retinal ganglion cells (RGCs) in vitro and in vivo. Methods: For in vivo studies, a unilateral optic nerve crush mouse model was established. Then, 100 mM Y-27632 (a ROCK inhibitor) or saline was applied to the experimental eyes once a day for 14 days. The effects of the ROCK inhibitor were evaluated by counting the surviving RGCs in the enucleated flat retina tissues and measuring the inner retinal thickness using optical coherence tomography (OCT), the amplitude of the electroretinogram (ERG), and the change in intraocular pressure (IOP). For the in vitro study, RGCs were isolated from five-day-old mice using a modified immunopanning method with magnetic beads. The isolated RGCs were incubated for 72 h with various concentrations of Y-27632, after which TUNEL assays were performed to determine the number of surviving RGCs. Results: Y-27632 has neuroprotective effects, as it significantly increased the number of surviving RGCs by approximately 6.3%. OCT and ERG data also revealed that Y-27632 induced neuroprotective effects in vivo; furthermore, Y-27632 reduced IOP by approximately 18.3%. The in vitro study revealed the dose-dependent neuroprotective effects of Y-27632, with the highest dose of Y-27632 (1000 nM) increasing the RGC survival rate after 72 h of incubation compared with that of the control. Conclusions: The ROCK inhibitor Y-27632 may exert some neuroprotective effects on RGCs when it is used as an eye drop through an IOP-independent mechanism. Full article

Dopaminergic amacrine cells (DACs) are a subclass of amacrine cells that modulate retinal processing and light adaptation by releasing dopamine. Although the role of dopamine is largely conserved, their retinal distribution across mammals remains incompletely characterized. In mice, rats, thirteen-lined ground squirrels (TLGSs), and macaques, we systematically compared the localization, number, and topography of DACs by their expression of tyrosine hydroxylase (TH), a crucial enzyme in the biosynthesis of dopamine. In all species examined, TH+ cells were primarily located in the inner nuclear layer; however, there was a species-dependent influence on their number and distribution. Mice exhibited the highest density of TH+cells but completely lacked displaced TH+cells (dTH+cells) in the ganglion cell layer. Despite interspecies variation in the total number of TH+cells in the retina, the overall density in rats, TLGSs, and macaques was similar. Most species displayed a higher density of DACs toward central retinal regions. However, rats exhibited a distinctive dorsal concentration, particularly among dTH+cells. Although most species examined exhibited a similar ratio of TH+cells to Brn3a+ retinal ganglion cells, TLGSs showed a marked reduction, indicating a potentially diminished dopaminergic modulatory role. Species-specific DAC topographies aligned with specialized visual regions, such as the visual streak in TLGS and the macula in macaques. These results reveal both conserved and divergent features of retinal dopamine circuitry, reflecting evolutionary adaptations to visual processing demands. Full article

Background/Objective: The Rs1 exon-1-del rat (Rs1KO) XLRS model shows normal retinal development until postnatal day 12 (P12) when small cystic spaces start to form in the inner nuclear layer. These enlarge rapidly, peak at P15, and then collapse by P19. These events overlap with eye opening at P12–P15. We investigated whether new light-driven retinal activity could contribute to the appearance and progression of schisis cavities in this rat model of XLRS disease. Methods: For dark rearing (D/D), mating pairs of Rs1KO strain were raised in total darkness in a special vivarium at UC Davis. When pups were born, they were maintained in total darkness, and eyes were collected at P12, P15, and P30 (n = 3/group) for each of the D/D and cyclic light-reared 12 h light–12 h dark (L/D) Rs1KO and wild-type (WT) littermates. Eyes were fixed, paraffin-embedded, and sectioned. Tissue morphology was examined by H&E and marker expression of retinoschisin1 (Rs1), rhodopsin (Rho), and postsynaptic protein 95 (Psd95) by fluorescent immunohistochemistry. H&E-stained images were analyzed with ImageJ version 1.54h to quantify cavity size using the “Analyze Particles” function. Results: Small intra-retinal schisis cavities begin to form by P12 in the inner retina of both D/D and L/D animals. Cavity formation was equivalent or more pronounced in D/D animals than in L/D animals. We compared Iba1 (activation marker of immune cells) distribution and found that by P12, when schisis appeared, Iba1⁺ cells had accumulated in regions of schisis. Iba1⁺ cells were more abundant in Rs1KO animals than WT animals and appeared slightly more prevalent in D/D- than L/D-reared Rs1KO animals. We compared photoreceptor development using Rho, Rs1, and Psd95 expression, and these were similar; however, the outer segments (OSs) of D/D animals with Rho labeling at P12 were longer than L/D animals. Conclusions: The results showed that cavities formed at the same time in D/D and L/D XLRS rat pups, indicating that the timing of schisis formation is not light stimulus-driven but rather appears to be a result of developmental events. Cavity size tended to be larger under dark-rearing conditions in D/D animals, which could be due to the decreased rate of phagocytosis by the RPE in the dark, allowing for continued growth of the OSs without the usual shedding of the distal tip, a key mechanism behind dark adaptation in the retina. These results highlight the complexity of XLRS pathology; however, we found no evidence that light-driven metabolic activity accounted for schisis cavity formation. Full article

Purpose: This study aims to evaluate the clinical utility of a prototype ultra-widefield (UWF) single-capture optical coherence tomography (OCT) lens developed to image large areas of the retina. Material and Methods: This study included OCT and angio-OCT measurements performed with a REVO FC 130 (Optopol Technology, Poland) with an add-on widefield lens in a case series of 215 patients with retinal pathologies and 39 healthy subjects. The imaging width provided by the lens was 22 mm (covering a 110-degree field of view), while the scanning window height ranged from 2.8 to 6 mm. Results: The quality of the peripheral UWF OCT and angio-OCT images obtained by REVO FC 130 with the attachable lens is very good and sufficient for patient diagnosis, follow-up, and treatment planning. Both the boundaries of the non-perfusion zones and the location and extent of vascular proliferations can be accurately traced. Furthermore, the vitreoretinal interface can also be accurately assessed over a large area. The imaging quality of the macula with UWF OCT angiography is also good. The mean thickness measurement difference between a UWF and a standard 10 mm 3D retinal scan in a healthy individuals for the Central ETDRS sector was −1.37 ± 2.96 µm (the 95% limits of agreement (LoA) on Bland–Altman plots ranged from −6.82 to 2.43); for the Inferior Inner sector, it was −2.81 ± 1.09 µm (95% LoA, −4.94 to −0.68); for the Inferior Outer sector, it was −1.31 ± 2.58 µm (95% LoA, −6.38 to 3.75); for the Nasal Inner sector: −1.46 ± 1.19 µm (95% LoA, −3.79 to 0.88); for the Nasal Outer sector, it was −0.56 ± 2.61 µm (95% LoA, −5.67 to 4.55); for the Superior Inner sector, it was −2.71 ± 3.16 µm (95% LoA, −8.91 to 3.48); for the Superior Outer sector, it was −1.82 ± 1.39 µm (95% LoA, −4.55 to 0.91); for the Temporal Inner sector, it was −1.77 ± 2.24 µm (95% LoA, −6.16 to 2.62); for the Temporal Outer sector, it was −3.61 ± 1.43 µm (95% LoA, −6.41 to −0.81). Discussion: The proposed method of obtaining UWF OCT and UWF angio-OCT images using an add-on lens with the REVO FC 130 gives high-quality scans over the entire 110-degree field of view. This study also shows a high agreement of the ETDRS sector’s thickness measurements between UWF and standard retinal scans, which allows UWF to be used for quantitative macular thickness analysis. Considering its image quality, simplicity, and reliability, an add-on lens can be successfully used for the UWF OCT and OCT angiography evaluation of the retina on a daily basis. Full article

Background: Adaptive optics transscleral flood illumination (AO-TFI) enables in vivo, non-invasive, high-resolution imaging of retinal pigment epithelium (RPE) and photoreceptor (PR) cells, paving the way for a new potential characterization of retinal diseases. This study aimed to analyze RPE and PR cells in a case of acute zonal occult outer retinopathy (AZOOR) using AO-TFI. Methods: A patient affected by AZOOR underwent a comprehensive eye examination, perimetry, electroretinography (ERG), autofluorescence, and optical coherence tomography (OCT) during the acute phase (T0). After three years (T1), OCT angiography (OCTA) and AO-TFI were also performed. Voronoi analysis was utilized to quantify RPE and PR cells. Results: At T0, OCT revealed interruptions in the ellipsoid zone (EZ) of the right eye, while the structure of the left eye appeared normal. Perimetry and ERG were abnormal in both eyes. At T1, OCT indicated recovery of the EZ in the right eye, while thinning of the ONL persisted. Perimetry and mfERG values remained below normative limits. OCTA exhibited globally reduced vessel density in the inner retina of the right eye. AO-TFI demonstrated reduced PR density in affected areas despite preserved EZ, while RPE cell density appeared unaffected. Conclusion: AO-TFI enabled a detailed visualization and quantification of macular RPE and PR cells, providing valuable insights into the pathophysiology of AZOOR. Full article

Diabetic retinopathy is a sight-threatening complication of diabetes mellitus, affecting millions of people worldwide. From a vascular perspective, diabetic retinopathy compromises the structure and function of the blood–retinal barrier, leading to aberrant angiogenesis and vascular leakage, with consequent loss of vision. This review will delve into the vascular abnormalities caused by diabetic retinopathy in the inner blood–retinal barrier, focusing primarily on retinal endothelial cells. It will then discuss how calcium signalling regulates inner blood–retina barrier function and dysfunction, how calcium channels contribute to the development of diabetic retinopathy, and how studying the components of the calcium toolkit may identify new therapeutic targets. Full article

Background: The retina plays a vital role in vision, and its impairment can cause significant visual deficits. Current retinal disease treatments range from conventional anti-inflammatory drugs to advanced anti-VEGF therapies and monoclonal antibodies. TnP, a novel synthetic peptide in preclinical development, has demonstrated therapeutic potential in chronic inflammatory conditions such as multiple sclerosis and asthma due to its immunomodulatory properties. Using zebrafish—which share significant genetic homology with humans—we investigated TnP’s effects on retinopathy models mimicking diabetic retinopathy (DR) through either cobalt chloride (CoCl₂)-induced hypoxia or light-induced retinal damage (LIRD). Methods: We employed two retinal injury models (CoCl₂-induced hypoxia and LIRD) and subjected them to TnP treatment, assessing the outcomes through visual–motor response testing and histological examination. Results: CoCl₂ exposure impaired swimming activity, while light damage reduced the movement distance. Both models induced distinct retinal morphological changes. Although TnP failed to reverse most injury effects, it specifically restored the inner plexiform layer (IPL)’s thickness. Conclusions: Our findings suggest that TnP may enhance neuronal plasticity by promoting cell proliferation and synaptic connectivity. While showing promise as a therapeutic candidate for retinal and neurodegenerative disorders, TnP might achieve optimal efficacy when combined with complementary treatments. Full article

Myo/Nog cells play a pivotal role in ocular development and demonstrate a rapid response to stress and injury. This study investigates their behavior and distribution in a murine model of retinitis pigmentosa, specifically in C3H/HeJ mice, which exhibit photoreceptor degeneration due to a homozygous mutation in the Pde6brd1 gene. Retinal samples from C3H/HeJ and C57BL/6J mice were analyzed at postnatal weeks 2.5 to 6 using hematoxylin and eosin staining, immunofluorescence for brain-specific angiogenesis inhibitor 1 (BAI1) expressed in Myo/Nog cells, and TUNEL labeling for apoptotic cell detection. The results demonstrated a progressive thinning of the outer nuclear layer (ONL) in C3H mice, accompanied by a significant increase in Myo/Nog cell numbers. In normal retinas, Myo/Nog cells were primarily located in the inner nuclear and outer plexiform layers. However, in C3H/HeJ mice, they accumulated in the ONL near apoptotic photoreceptors and within the choroid. Notably, in these degenerative regions, Myo/Nog cells exhibited features of phagocytosis, suggesting a role in apoptotic cell clearance. Additionally, parallels between Myo/Nog cell responses in retinitis pigmentosa and models of oxygen-induced retinopathy, ocular hypertension, and light damage suggest that these cells may be leveraged for therapeutic purposes. Full article

Retinal ischemic disorders present significant threats to vision, characterized by inadequate blood supply oxygen–glucose deprivation (OGD), oxidative stress, and cellular injury, often resulting in irreversible injury. Catalpol, an iridoid glycoside derived from Rehmannia glutinosa, has demonstrated antioxidative and neuroprotective effects. This study aimed at investigating the protective effects and mechanisms of catalpol against oxidative stress or OGD in vitro and retinal ischemia in vivo, focusing on the modulation of key biomarkers of retinal ischemia, including HIF-1α, vascular endothelial growth factor (VEGF), angiopoietin-2, MCP-1, and the Wnt/β-catenin pathway. Cellular viability was assessed using retinal ganglion cell-5 (RGC-5) cells cultured in DMEM; a 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was performed. H₂O₂ (1 mM)/OGD was utilized. Vehicle or different catalpol concentrations were administered 15 min before the ischemic-like insults. The Wistar rat eyes’ intraocular pressure was increased to 120 mmHg for 60 min to induce retinal ischemia. Intravitreous injections of catalpol (0.5 or 0.25 mM), Wnt inhibitor DKK1 (1 μg/4 μL), anti-VEGF Lucentis (40 μg/4 μL), or anti-VEGF Eylea (160 μg/4 μL) were administered to the rats’ eyes 15 min before or after retinal ischemia. Electroretinogram (ERG), fluorogold retrograde labeling RGC, Western blotting, ELISA, RT-PCR, and TUNEL were utilized. In vitro, both H₂O₂ and OGD models significantly (p < 0.001/p < 0.001; H₂O₂ and OGD) induced oxidative stress/ischemic-like insults, decreasing RGC-5 cell viability (from 100% to 55.14 ± 2.19%/60.84 ± 4.57%). These injuries were insignificantly (53.85 ± 1.28% at 0.25 mM)/(63.46 ± 3.30% at 0.25 mM) and significantly (p = 0.003/p = 0.012; 64.15 ± 2.41%/77.63 ± 8.59% at 0.5 mM) altered by the pre-administration of catalpol, indicating a possible antioxidative and anti-ischemic effect of 0.5 mM catalpol. In vivo, catalpol had less effect at 0.25 mM for ERG amplitude ratio (median [Q1, Q3] 14.75% [12.64%, 20.48%]) and RGC viability (mean ± SE 63.74 ± 5.13%), whereas (p < 0.05 and p < 0.05) at 0.5 mM ERG’s ratio (35.43% [24.35%, 43.08%]) and RGC’s density (74.34 ± 5.10%) blunted the ischemia-associated significant (p < 0.05 and p < 0.01) reduction in ERG b-wave amplitude (6.89% [4.24%, 10.40%]) and RGC cell viability (45.64 ± 3.02%). Catalpol 0.5 mM also significantly protected against retinal ischemia supported by the increased amplitude ratio of ERG a-wave and oscillatory potential, along with recovering a delayed a-/b-wave response time ratio. When contrasted with DKK1 or Lucentis, catalpol exhibited similar protective effects against retinal ischemia via significantly (p < 0.05) blunting the ischemia-induced overexpression of β-catenin, VEGF, or angiopoietin-2. Moreover, ischemia-associated significant increases in apoptotic cells in the inner retina, inflammatory biomarker MCP-1, and ischemic indicator HIF-1α were significantly nullified by catalpol. Catalpol demonstrated antiapoptotic, anti-inflammatory, anti-ischemic (in vivo retinal ischemia or in vitro OGD), and antioxidative (in vitro) properties, counteracting retinal ischemia via suppressing upstream Wnt/β-catenin and inhibiting downstream HIF-1α, VEGF, and angiopoietin-2, together with its decreasing TUNEL apoptotic cell number and inflammatory MCP-1 concentration. Full article

Objectives: In this study, the objective was to assess the correlation between macular function and peripapillary retinal nerve fiber layer (pRNFL) thickness following successful rhegmatogenous retinal detachment (RRD) surgery, as well as the subsequent recovery of visual acuity. Methods: This was a cross-sectional study including 64 eyes from patients with RRD who underwent successful treatment with 23G pars plana vitrectomy (PPV), endophotocoagulation and sulfur-hexafluoride (SF6) were included and compared to a control group consisting of 136 healthy eyes. A complete ophthalmological examination was performed on all participants, including assessment of macular sensitivity using macular integrity assessment (MAIA) microperimetry and pRNFL thickness using DRI-Triton swept-source (SS)–optical coherence tomography (OCT). Results: In the RRD group, retinal sensitivity was decreased. The temporal (T) sector of the total retina (TR) protocol was thicker, while the superior (S) and inferior (I) sectors of the pRNFL protocol were thinner. Within the RRD group, positive correlations were observed between the nasal (N), I sectors and total thickness of TR protocol and MAIA inferior outer (IO) sector; the I sector and total thickness of the TR protocol and MAIA inferior inner (II) sector; the I sector of the pRNFL protocol and MAIA IO sector. Negative correlations were shown between the S, T sectors and total thickness of the pRNFL protocol and MAIA central (C) sector; the N sector and total thickness of the pRNFL protocol and MAIA central temporal (CT) sector. Conclusions: RRD leads to a decrease in pRNFL thickness accompanied by reduced macular sensitivity. These changes may be attributed to factors such as the specific location of the RRD, the distribution pattern of the RNFL and the chosen surgical approach. Full article

Paracentral acute middle maculopathy (PAMM) is a macular condition primarily detected using optical coherence tomography (OCT) imaging. It presents as hyperreflective bands within the inner nuclear layer (INL) of the retina, often leading to localized degenerative phenomena. PAMM is a condition that reveals a dysfunction in the microvascular network of the retina. However, it is not an isolated phenomenon but rather an indicator of deeper and even systemic, prevalently vascular-related issues related to a wide array of conditions that impact circulation, including retinal vein and artery occlusion, diabetic retinopathy, and hypertensive retinal vascular changes. PAMM occurs due to impaired perfusion within the retinal deep capillary plexus, clinically leading to subtle but noticeable blind spots (scotomas) in the central visual field. Recent advances in imaging technology, particularly optical coherence tomography angiography (OCTA), have provided a clearer view of the underlying vascular alterations. Thus, PAMM may currently serve as a biomarker in broader ocular and systemic pathologies before disease progression. This review explores the latest reports in the literature on PAMM, from its characteristic imaging features to the evolving theories behind its development. By bridging the gap between ophthalmology and systemic health, PAMM may facilitate earlier diagnosis and tailored management strategies for conditions that extend far beyond the eye. Understanding this entity could ultimately transform our approach to assessing vascular health toward further research, risk prediction, and patient care. Full article

Objectives: We sought to investigate the visual function, retinal features, and genotype–phenotype correlations of an Australian cohort of RPGR carriers. Methods: In this cross-sectional study, we evaluated RPGR carriers seen in Melbourne and Perth between 2013 and 2023 and healthy women seen between 2022 and 2023 in Melbourne. Visual acuity tests, fundus-tracked microperimetry, and retinal imaging were performed. RPGR carriers were classified into four retinal phenotypes (normal, radial, focal pigmentary retinopathy, and male pattern phenotype) and compared against healthy controls. Genotype–phenotype relationships in the RPGR carriers were investigated. Results: Thirty-five female RPGR carriers and thirty healthy controls were included in this study. The median ages were 40 and 48.5 years for RPGR carriers and controls, respectively (p = 0.26). Most RPGR carriers (89%) had a genetic diagnosis. Best-corrected visual acuity (BCVA), low luminance visual acuity, retinal sensitivity, central inner retinal thickness (IRT, 1°), and photoreceptor complex (PRC) thickness across the central 1–7° of the retina differed between phenotypes of RPGR carriers. On average, RPGR carriers with ORF15 variants (n = 25 carriers) had reduced LLVA, a greater IRT at 1°, and thinner PRC thickness at 7° from the fovea (all p < 0.05) compared to those with exon 1–14 variants. Conclusions: Female RPGR carriers with severe retinal phenotypes had significantly decreased visual function and changes in retinal structure in comparison to both the controls and carriers with mild retinal disease. BCVA, LLVA, retinal sensitivity, and retinal thickness are biomarkers for detecting retinal disease in RPGR carriers. The genetic variant alone did not influence retinal phenotype; however, RPGR carriers with ORF15 variants exhibited reduced retinal and visual measurements compared to those with exon 1–14 variants. Full article

The retinal structure is generally conserved across vertebrates; however, variations occur due to the relationship between environmental factors and visual perception. Birds have adapted to diverse ecological contexts, evolving specialized visual characteristics. In this study, we examined the retina of Audouin’s Gull (Larus audouinii) using light and transmission electron microscopy. This species is particularly intriguing as it is considered an outlier within the Laridae family: despite being a diurnal bird, it exhibits nocturnal/crepuscular foraging behaviour. Our analysis revealed a retina well adapted for diurnal activity, with features such as a retinal thickness comparable to that of other diurnal birds, a well-developed retinal pigment epithelium, and a high cone-to-rod density ratio. However, we also observed characteristics aligned with nocturnal or crepuscular activity, including a slightly increased rod density in central regions and the presence of two distinct types of horizontal cells in the inner nuclear layer. Additionally, the inner retina showed evidence of complex visual processing. These findings suggest that Audouin’s Gull is an excellent model for visual ecology studies due to its specialized adaptations. Full article

This study evaluated the neuroprotective potential of peptain-1 conjugated to a cell-penetrating peptide (CPP-P1) in an ocular hypertension model of glaucoma. Brown Norway (BN) rats were subjected to intraocular pressure (IOP) elevation via intracameral injection of silicone oil (SO), with concurrent intravitreal injections of either CPP-P1 or a vehicle. Retinal cross-sections were analyzed for markers of neuroprotection, including cAMP response element-binding protein (CREB), phosphorylated CREB (p-CREB), growth-associated protein-43 (GAP43), synapsin-1 (SYN1), and superoxide dismutase 2 (SOD2). Hematoxylin and eosin staining was used to assess retinal-layer thickness. SO-treated rats exhibited significant reductions in the thickness of the inner nuclear layer (INL, 41%, p = 0.016), inner plexiform layer (IPL, 52%, p = 0.0002), and ganglion cell layer (GCL, 57%, p = 0.001). CPP-P1 treatment mitigated these reductions, preserving INL thickness by 32% (p = 0.059), IPL by 19% (p = 0.119), and GCL by 31% (p = 0.057). Increased levels of CREB (p = 0.17) and p-CREB (p = 0.04) were observed in IOP-elevated, CPP-P1-treated retinas compared to IOP-elevated, vehicle-treated retinas. Although overall GAP43 levels were low, there was a modest increase in expression within the IPL and GCL in SO- and CPP-P1-treated retinas (p = 0.15 and p = 0.09, respectively) compared to SO- and vehicle-treated retinas. SO injection reduced SYN1 expression in both IPL and GCL (p = 0.01), whereas CPP-P1 treatment significantly increased SYN1 levels in the IPL (p = 0.03) and GCL (p = 0.002). While SOD2 expression in the GCL was minimal across all groups, a trend toward increased expression was observed in CPP-P1-treated animals (p = 0.16). The SO model was replicated with SO removal after 7 days and monitored for 21 days followed by retinal flat-mount preparation to assess retinal ganglion cell (RGC) survival. A 42% loss in RGCs (p = 0.009) was observed in SO-injected eyes, which were reduced by approximately 37% (p = 0.03) with CPP-P1 treatment. These findings suggest that CPP-P1 is a promising neuroprotective agent that promotes retinal ganglion cell survival and the preservation of other retinal neurons, potentially through enhanced CREB signaling in a rat model of SO-induced ocular hypertension. Full article

Myopic eye growth induces mechanical stretch, which can lead to structural and functional retinal alterations. Here, we investigated the effect of lens-induced myopic growth on the distribution of retinal ganglion cells (RGCs), glial fibrillary acidic protein (GFAP) expression and intensity, and peripapillary retinal nerve fiber layer (ppRNFL) thickness in common marmosets (Callithrix jacchus) induced with myopia continuously for six months, using immunohistochemistry and spectral-domain optical coherence tomography. We also explored the relationship between cellular structural parameters and the photopic negative response (PhNR) using full-field electroretinography. Marmosets induced with myopia for six months developed axial myopia, had a thinner ppRNFL, reduced peripapillary ganglion cell (≈20%) and astrocyte density (≈42%), increased panretinal GFAP expression (≈42%) and nasal mid-periphery staining intensity (≈81%) compared to age-matched controls. Greater degrees of myopia and vitreous elongation were associated with reduced peripapillary RGCs and astrocyte density, and increased GFAP expression and intensity. These cellular structural changes did not show a significant relationship with the features of the PhNR, which remained unchanged. The outcomes of this study suggest that myopia induces a reorganization of the peripapillary inner retina at the cellular level that may not result in measurable functional repercussions at this stage of myopia development. Full article