ArticleCell reports2019
Partial Cone Loss Triggers Synapse-Specific Remodeling and Spatial Receptive Field Rearrangements in a Mature Retinal Circuit.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Dysfunction of α2δ4 leads to photoreceptor degeneration through disrupted synaptic mitochondria and calcium crosstalk.Cell death & disease · 2026Article
- Microglial regulation of synaptic plasticity in transsynaptic degeneration of glaucoma.Frontiers in neuroscience · 2026Review
- Afadin-deficient mouse retinas exhibit severe neuronal lamination defects but preserve visual functions.eLife · 2025Article
- Retinal Impairments in Mice Lacking Both Nxnl1 and Nxnl2 Genes.Investigative ophthalmology & visual science · 2025Article
- Photoreceptor degeneration has heterogeneous effects on functional retinal ganglion cell types.The Journal of physiology · 2025Article
- Genome-edited retinal organoids restore host bipolar connectivity in the primate macula.bioRxiv : the preprint server for biology · 2025Article
- Divergent mechanisms of neural adaptation and instability in the mammalian retina.Current biology : CB · 2025Article
- Cellular and circuit remodeling of the primate foveal midget pathway after acute photoreceptor loss.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Cellular and Molecular Mechanisms Regulating Retinal Synapse Development.Annual review of vision science · 2024Review
- Retinoic Acid-Dependent Loss of Synaptic Output from Bipolar Cells Impairs Visual Information Processing in Inherited Retinal Degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- A pupillary contrast response in mice and humans: Neural mechanisms and visual functions.Neuron · 2024Article
- Targeting miR-181a/b in retinitis pigmentosa: implications for disease progression and therapy.Cell & bioscience · 2024Article
- Losing, preserving, and restoring vision from neurodegeneration in the eye.Current biology : CB · 2023Review
- Neural and Müller glial adaptation of the retina to photoreceptor degeneration.Neural regeneration research · 2023Review
- Off Starburst Amacrine Cells in the Retina Trigger Looming-Evoked Fear Responses in Mice.eNeuro · 2023Article
- Asymmetric retinal direction tuning predicts optokinetic eye movements across stimulus conditions.eLife · 2023Article
- Article
- Retinoic acid inhibitors mitigate vision loss in a mouse model of retinal degeneration.Science advances · 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
- Inhibition, but not excitation, recovers from partial cone loss with greater spatiotemporal integration, synapse density, and frequency.Cell reports · 2022Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Resilience of neural circuits has been observed in the persistence of function despite neuronal loss. In vision, acuity and sensitivity can be retained after 50% loss of cones. While neurons in the cortex can remodel after input loss, the contributions of cell-type-specific circuits to resilience are unknown. Here, we study the effects of partial cone loss in mature mouse retina where cell types and connections are known. At first-order synapses, bipolar cell dendrites remodel and synaptic proteins diminish at sites of input loss. Sites of remaining inputs preserve synaptic proteins. Second-order synapses between bipolar and ganglion cells remain stable. Functionally, ganglion cell spatio-temporal receptive fields retain center-surround structure following partial cone loss. We find evidence for slower temporal filters and expanded receptive field surrounds, derived mainly from inhibitory inputs. Surround expansion is absent in partially stimulated control retina. Results demonstrate functional resilience to input loss beyond pre-existing mechanisms in control retina.
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