ArticleMolecular vision2009
Evaluation of the adeno-associated virus mediated long-term expression of channelrhodopsin-2 in the mouse retina.
Article in Molecular vision, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Inducible CreEReNeuro · 2026Article
- AAV dose-dependent transduction efficiency in retinal ganglion cells and functional efficacy of optogenetic vision restoration.Gene therapy · 2024Article
- Optogenetic targeting of AII amacrine cells restores retinal computations performed by the inner retina.Molecular therapy. Methods & clinical development · 2023Article
- Highly sensitive visual restoration and protection via ectopic expression of chimeric rhodopsin in mice.iScience · 2023Article
- Optogenetic Therapy for Visual Restoration.International journal of molecular sciences · 2022Review
- Optogenetic Strategies for Vision Restoration.Advances in experimental medicine and biology · 2021Review
- Retinal Prosthetic Approaches to Enhance Visual Perception for Blind Patients.Micromachines · 2020Review
- Effects of AAV2-mediated co-transfection of CTGF and TIMP1 genes on degenerative lumbar intervertebral discs in rhesus monkeys in vivo.American journal of translational research · 2018Article
- Tropism of engineered and evolved recombinant AAV serotypes in the rd1 mouse and ex vivo primate retina.Gene therapy · 2017Article
- Long-term expression of melanopsin and channelrhodopsin causes no gross alterations in the dystrophic dog retina.Gene therapy · 2017Article
- Developmental suppression of forebrain trkA receptors and attentional capacities in aging rats: A longitudinal study.Behavioural brain research · 2017Article
- Visual Responses of Photoreceptor-Degenerated Rats Expressing Two Different Types of Channelrhodopsin Genes.Scientific reports · 2017Article
- Dampening Spontaneous Activity Improves the Light Sensitivity and Spatial Acuity of Optogenetic Retinal Prosthetic Responses.Scientific reports · 2016Article
- Disruption in dopaminergic innervation during photoreceptor degeneration.The Journal of comparative neurology · 2016Article
- Maintaining ocular safety with light exposure, focusing on devices for optogenetic stimulation.Vision research · 2016Article
- Biophysical Properties of Optogenetic Tools and Their Application for Vision Restoration Approaches.Frontiers in systems neuroscience · 2016Review
- Viral-mediated Ntf3 overexpression disrupts innervation and hearing in nondeafened guinea pig cochleae.Molecular therapy. Methods & clinical development · 2016Article
- Photochemical approaches to vision restoration.Vision research · 2015Review
- Increased phosphorylation of Cx36 gap junctions in the AII amacrine cells of RD retina.Frontiers in cellular neuroscience · 2015Article
- Vector platforms for gene therapy of inherited retinopathies.Progress in retinal and eye research · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe conversion of inner retinal neurons to photosensitive cells via viral mediated expression of channelrhodopsin-2 (ChR2) offers a new potential approach for the restoration of vision after photoreceptor degeneration. This study was conducted to evaluate the recombinant adeno-associated virus serotype 2 (rAAV2)-mediated long-term expression and safety of ChR2 in the mouse retina.
methodsrAAV2 vectors carrying a fusion construct of channelopsin-2 (Chop2) and green fluorescent protein (GFP; Chop2-GFP) under the control of a hybrid cytomegalovirus early enhancer and chicken beta-actin (CAG) promoter were injected at different concentrations into the eyes of wild-type adult mice. The retinas were harvested up to 18 months after virus injection for immunostaining and electrophysiological studies. Injected mice were kept either under normal light conditions, or exposed to a strong blue light. The expression of GFP and the density of the cells in the ganglion cell layer (GCL) were examined.
resultsThe expression of Chop2-GFP was stable for up to 18 months. Chop-GFP was observed predominantly in retinal ganglion as well as amacrine cells. At the highest virus concentration (6 x 10(12) GC/ml), up to 20% of the cells in the GCL were infected by the virus. At the lowest virus concentration (1 x 10(10) GC/ml), the expression was targeted to AII amacrine cells. The concentration of the virus, the light conditions, and the percentage of Chop2-GFP-positive cells had no effect on the density and, thus, on the survival of the cells in the GCL. Sufficient number of functional ChR2 channels were maintained in ganglion cells to drive robust membrane depolarization and spike firing in response to light.
conclusionsExpression of Chop2-GFP could be achieved in retinal neurons in vivo for the duration of the lifespan of mice. The expression of Chop2-GFP did not cause any detectable toxicity and cell death to neurons of the ganglion cell layer.
Indexed as
Identifiers
19710944PMC2730750W2105249592What OpenQuestion holds
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.