LiGluR restores visual responses in rodent models of inherited blindness
Open accessAbstract
Inherited retinal degeneration results from many different mutations in either photoreceptor-specific or nonphotoreceptor-specific genes. However, nearly all mutations lead to a common blinding phenotype that initiates with rod cell death, followed by loss of cones. In most retinal degenerations, other retinal neuron cell types survive for long periods after blindness from photoreceptor loss. One strategy to restore light responsiveness to a retina rendered blind by photoreceptor degeneration is to express light-regulated ion channels or transporters in surviving retinal neurons. Recent experiments in rodents have restored light-sensitivity by expressing melanopsin or microbial opsins either broadly throughout the retina or selectively in the inner segments of surviving cones or in bipolar cells. Here, we present an approach whereby a genetically and chemically engineered light-gated ionotropic glutamate receptor (LiGluR) is expressed selectively in retinal ganglion cells (RGCs), the longest-surviving cells in retinal blinding diseases. When expressed in the RGCs of a well-established model of retinal degeneration, the rd1 mouse, LiGluR restores light sensitivity to the RGCs, reinstates light responsiveness to the primary visual cortex, and restores both the pupillary reflex and a natural light-avoidance behavior.
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Pre-clinical optogenetic trials in mouse models of retinitis pigmentosa have restored basic visual function in blind animals, providing proof of principle.
“Pre-clinical trials of optogenic therapies in murine models of retinitis pigmentosa have provided proof-of-principle in restoring basic visual function to blind animals, and human clinical trials are currently underway.”
From Correcting visual loss by genetics and prosthetics (2020) · cites this paper as Caporale 2011
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- Authors
- Caporale, N., Kolstad, K. D., Lee, T., Tochitsky, I., Dalkara, D., Trauner, D., Kramer, R., Dan, Y., Isacoff, E. Y., & Flannery, J. G.
- Affiliations
- University of California, Berkeley (US)
- Ludwig-Maximilians-Universität München (DE)
- Howard Hughes Medical Institute (US)
- Lawrence Berkeley National Laboratory (US)
- Corresponding author
- Flannery, John G
- ORCID
- Venue
- Molecular Therapy
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 19
- Issue
- 7
- Pages
- 1212-1219
- ISSN
- 1525-0016 (ISSN-L)
- PMC
- PMC3129552
- OpenAlex
- W2017787995
- Cited by
- 182
- References
- 46
- Citations by year
- 2026: 6 · 2025: 7 · 2023: 6 · 2022: 14 · 2021: 5 · 2020: 9 · 2019: 10 · 2018: 12 · 2017: 19 · 2016: 9 · 2015: 24 · 2014: 19 · 2013: 22 · 2012: 14
- FWCI
- 7.91
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Molecular Therapy (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Eye Institute (PN2EY018241, R01EY014375)
- National Institute of General Medical Sciences (T32GM066698, T32GM007232)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Photoreceptor and optogenetics research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neural Engineering
- Keywords
- inherited retinal degeneration, retinal ganglion cells, rd1 mouse, photoreceptor degeneration, visual cortex responses, pupillary reflex, retinal prosthesis, gene therapy
- MeSH terms
- Dependovirus, Animals, Blindness, Electroretinography, Light, Mice, Inbred C57BL, Retinal Ganglion Cells, Visual Cortex, Receptors, Glutamate, Mice
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