Age-related alterations in neurons of the mouse retina
Open accessAbstract
The behavioral consequences of age-related alterations in neural function are well documented, but less is known about their cellular bases. To characterize such changes, we analyzed 14 molecularly identified subsets of mouse retinal projection neurons (retinal ganglion cells or RGCs) and interneurons (amacrine, bipolar, and horizontal cells). The retina thinned but expanded with age, maintaining its volume. There was minimal decline in the number of RGCs, interneurons, or photoreceptors, but the diameter of RGC dendritic arbors decreased with age. Together, the increased retinal area and the decreased dendritic area may lead to gaps in RGC coverage of the visual field. Axonal arbors of RGCs in the superior colliculus also atrophied with age, suggesting that the relay of visual information to central targets may decline over time. On the other hand, the laminar restriction of RGC dendrites and the interneuronal processes that synapse on them were not detectably disturbed, and RGC subtypes exhibited distinct electrophysiological responses to complex visual stimuli. Other neuronal types aged in different ways: amacrine cell arbors did not remodel detectably, whereas horizontal cell processes sprouted into the photoreceptor layer. Bipolar cells showed arbor-specific alterations: their dendrites sprouted but their axons remained stable. In summary, retinal neurons exhibited numerous age-related quantitative alterations (decreased areas of dendritic and axonal arbors and decreased density of cells and synapses), whereas their qualitative features (molecular identity, laminar specificity, and feature detection) were largely preserved. Together, these data reveal selective age-related alterations in neural circuitry, some of which could underlie declines in visual acuity.
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Old mice develop opaque lenses and lose retinal ganglion cells in the innermost retinal layer.
“Old mice develop opaque lenses and lose retinal ganglion cells (RGCs) in the innermost retinal layer (Calkins, 2013; Downs, 2015; Samuel et al., 2011; Wolf et al., 2000) (Figure 7J).”
From Loss of epigenetic information as a cause of mammalian aging (2023) · cites this paper as Samuel et al., 2011
The Discussion mentions lens opacification as an age-related optical factor, but does not establish that the study's old mice developed opaque lenses. More decisively, the Results section, “Neurons are preserved in old retina,” reports little change in retinal neuron numbers and no detectable age-related increase in cell death, contrary to the claim that old mice lose RGCs. (LLM, conf=0.90)
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- Authors
- Samuel, M. A., Zhang, Y., Meister, M., & Sanes, J. R.
- Affiliations
- Harvard University (US)
- Corresponding author
- Sanes, Joshua R.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-11-02
- Volume
- 31
- Issue
- 44
- Pages
- 16033-16044
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3238393
- OpenAlex
- W2117429439
- Cited by
- 184
- References
- 71
- Citations by year
- 2026: 5 · 2025: 21 · 2024: 14 · 2023: 23 · 2022: 17 · 2021: 13 · 2020: 11 · 2019: 10 · 2018: 8 · 2017: 11 · 2016: 8 · 2015: 17 · 2014: 11 · 2013: 9 · 2012: 6
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by)
- Funders
- Damon Runyon Cancer Research Foundation
- National Institutes of Health
- National Institute on Aging (R01AG032322)
- National Institute of Neurological Disorders and Stroke (R01NS029169)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Visual perception and processing mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- retinal aging, retinal ganglion cells, amacrine cells, bipolar cells, horizontal cells, superior colliculus, retinal interneurons, photoreceptors, synaptic density, visual acuity loss, mouse retina, neural circuits
- MeSH terms
- Age Factors, Aging, Animals, Axons, Dendrites, Eye Proteins, Female, Flow Cytometry, Gene Expression Regulation, Immunoglobulins, Luminescent Proteins, Male, Membrane Potentials, Mice, Inbred C57BL, Mice, Transgenic, Nerve Tissue Proteins, Neurons, Retina, Retinal Ganglion Cells, Visual Pathways, Cell Adhesion Molecules, Patch-Clamp Techniques, Thy-1 Antigens, Photoreceptor Cells, Vertebrate, Amacrine Cells, Mice, Junctional Adhesion Molecule B, In Vitro Techniques
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