ArticleDevelopmental neurobiology2014
Retinal regeneration is facilitated by the presence of surviving neurons.
Article in Developmental neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
52 citing papers in PubMed, 70 citations in OpenAlex.
- Müller glial and microglial responses coupled to recovery of cone photoreceptors following limited cone ablation in zebrafish retina.Scientific reports · 2026Article
- Article
- Microglia response and function in a chronic model of photoreceptor damage.Frontiers in cell and developmental biology · 2025Article
- Review
- New pathways to neurogenesis: Insights from injury-induced retinal regeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Forced MyD88 signaling in microglia impacts the production and survival of regenerated retinal neurons.Frontiers in cell and developmental biology · 2024Article
- Cytokines IL-1β and IL-10 are required for Müller glia proliferation following light damage in the adult zebrafish retina.Frontiers in cell and developmental biology · 2024Article
- Intrinsic and Induced Neuronal Regeneration in the Mammalian Retina.Antioxidants & redox signaling · 2023Review
- Cell-Based Therapies: Strategies for Regeneration.Cold Spring Harbor perspectives in medicine · 2023Review
- Characterization of Macroglia Response during Tissue Repair in a Laser-Induced Model of Retinal Degeneration.International journal of molecular sciences · 2023Article
- Necroptosis plays a crucial role in the exacerbation of retinal injury after blunt ocular trauma.Neural regeneration research · 2023Article
- Assessing Rewiring of the Retinal Circuitry by Electroretinogram (ERG) After Inner Retinal Lesion in Adult Zebrafish.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Generating Widespread and Scalable Retinal Lesions in Adult Zebrafish by Intraocular Injection of Ouabain.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Eye flukes (Diplostomum spp) damage retinal tissue and may cause a regenerative response in wild threespine stickleback fish.Experimental eye research · 2022Article
- Cell Sources for Retinal Regeneration: Implication for Data Translation in Biomedicine of the Eye.Cells · 2022Review
- Comparative Biology of Vertebrate Retinal Regeneration: Restoration of Vision through Cellular Reprogramming.Cold Spring Harbor perspectives in biology · 2022Review
- Pigment Epithelia of the Eye: Cell-Type Conversion in Regeneration and Disease.Life (Basel, Switzerland) · 2022Review
- Dynamic functional and structural remodeling during retinal regeneration in zebrafish.Frontiers in molecular neuroscience · 2022Article
- Eyes on CHARGE syndrome: Roles of CHD7 in ocular development.Frontiers in cell and developmental biology · 2022Review
- Zebrafish models of inherited retinal dystrophies.Journal of translational genetics and genomics · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Teleost fish regenerate their retinas after damage, in contrast to mammals. In zebrafish subjected to an extensive ouabain-induced lesion that destroys all neurons and spares Müller glia, functional recovery and restoration of normal optic nerve head (ONH) diameter take place at 100 days postinjury. Subsequently, regenerated retinas overproduce cells in the retinal ganglion cell (RGC) layer, and the ONH becomes enlarged. Here, we test the hypothesis that a selective injury, which spares photoreceptors and Müller glia, results in faster functional recovery and fewer long-term histological abnormalities. Following this selective retinal damage, recovery of visual function required 60 days, consistent with this hypothesis. In contrast to extensively damaged retinas, selectively damaged retinas showed fewer histological errors and did not overproduce neurons. Extensively damaged retinas had RGC axons that were delayed in pathfinding to the ONH, and showed misrouted axons within the ONH, suggesting that delayed functional recovery following an extensive lesion is related to defects in RGC axons exiting the eye and/or reaching their central targets. The atoh7, fgf8a, Sonic hedgehog (shha), and netrin-1 genes were differentially expressed, and the distribution of hedgehog protein was disrupted after extensive damage as compared with selective damage. Confirming a role for Shh signaling in supporting rapid regeneration, shha(t4) +/- zebrafish showed delayed functional recovery after selective damage. We suggest that surviving retinal neurons provide structural/molecular information to regenerating neurons, and that this patterning mechanism regulates factors such as Shh. These factors in turn control neuronal number, retinal lamination, and RGC axon pathfinding during retinal regeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.