ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Activation of Rod Input in a Model of Retinal Degeneration Reverses Retinal Remodeling and Induces Formation of Functional Synapses and Recovery of Visual Signaling in the Adult Retina.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Impact of Aii Amacrine Cell Rewiring in a Pathoconnectome-Based Computational Model of Early Retinal Degeneration.bioRxiv : the preprint server for biology · 2026Article
- Photoreceptor degeneration has heterogeneous effects on functional retinal ganglion cell types.The Journal of physiology · 2025Article
- A metabotropic glutamate receptor agonist enhances visual signal fidelity in a mouse model of retinitis pigmentosa.bioRxiv : the preprint server for biology · 2024Article
- Light regulation of rhodopsin distribution during outer segment renewal in murine rod photoreceptors.Current biology : CB · 2024Article
- Late gene therapy limits the restoration of retinal function in a mouse model of retinitis pigmentosa.Nature communications · 2023Article
- Cones and cone pathways remain functional in advanced retinal degeneration.Current biology : CB · 2023Article
- Late gene therapy limits the restoration of retinal function in a mouse model of retinitis pigmentosa.bioRxiv : the preprint server for biology · 2023Article
- Neural and Müller glial adaptation of the retina to photoreceptor degeneration.Neural regeneration research · 2023Review
- Extracting spacing-derived estimates of rod density in healthy retinae.Biomedical optics express · 2023Article
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- Insulin receptor activation by proinsulin preserves synapses and vision in retinitis pigmentosa.Cell death & disease · 2022Article
- Late-stage rescue of visually guided behavior in the context of a significantly remodeled retinitis pigmentosa mouse model.Cellular and molecular life sciences : CMLS · 2022Article
- Impact of Photoreceptor Loss on Retinal Circuitry.Annual review of vision science · 2021Review
- Substantial restoration of night vision in adult mice with congenital stationary night blindness.Molecular therapy. Methods & clinical development · 2021Article
- Retinal glial remodeling by FGF21 preserves retinal function during photoreceptor degeneration.iScience · 2021Article
- Restoration of mGluR6 Localization Following AAV-Mediated Delivery in a Mouse Model of Congenital Stationary Night Blindness.Investigative ophthalmology & visual science · 2021Article
- Microfluidic and Microscale Assays to Examine Regenerative Strategies in the Neuro Retina.Micromachines · 2020Review
- Article
- Energy Shortage in Human and Mouse Models of SLC4A11-Associated Corneal Endothelial Dystrophies.Investigative ophthalmology & visual science · 2020Article
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Authors and funding
8 authors.
Funding
Abstract
A major cause of human blindness is the death of rod photoreceptors. As rods degenerate, synaptic structures between rod and rod bipolar cells disappear and the rod bipolar cells extend their dendrites and occasionally make aberrant contacts. Such changes are broadly observed in blinding disorders caused by photoreceptor cell death and are thought to occur in response to deafferentation. How the remodeled retinal circuit affects visual processing following rod rescue is not known. To address this question, we generated male and female transgenic mice wherein a disrupted cGMP-gated channel (CNG) gene can be repaired at the endogenous locus and at different stages of degeneration by tamoxifen-inducible cre-mediated recombination. In normal rods, light-induced closure of CNG channels leads to hyperpolarization of the cell, reducing neurotransmitter release at the synapse. Similarly, rods lacking CNG channels exhibit a resting membrane potential that was ~10 mV hyperpolarized compared to WT rods, indicating diminished glutamate release. Retinas from these mice undergo stereotypic retinal remodeling as a consequence of rod malfunction and degeneration. Upon tamoxifen-induced expression of CNG channels, rods recovered their structure and exhibited normal light responses. Moreover, we show that the adult mouse retina displays a surprising degree of plasticity upon activation of rod input. Wayward bipolar cell dendrites establish contact with rods to support normal synaptic transmission, which is propagated to the retinal ganglion cells. These findings demonstrate remarkable plasticity extending beyond the developmental period and support efforts to repair or replace defective rods in patients blinded by rod degeneration.
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