ArticleDocumenta ophthalmologica. Advances in ophthalmology2017
Detailed electroretinographic findings in rd8 mice.
Article in Documenta ophthalmologica. Advances in ophthalmology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- CCR1 signaling as a common injury pathway in retinal degeneration.Journal of neuroinflammation · 2026Article
- Article
- A Controlled Impact of Optic Nerve as a New Model of Traumatic Optic Neuropathy in Mouse.Investigative ophthalmology & visual science · 2018Article
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Authors and funding
4 authors.
Funding
Abstract
purposePrevious work has suggested that the retinal degeneration mutant rd8 mouse lacks an electroretinographic (ERG) phenotype until about 9 months of age. We evaluated the ERG phenotype of these mice by measuring both conventional ERG responses and scotopic threshold responses.
methodsGroups of 4-month-old wild-type (WT) and mutant (rd8) mice were anesthetized and tested for mass retinal responses (ERGs) to several types of visual stimuli. Scotopic threshold responses were accumulated with brief scotopic flashes at a series of very dim intensities. Dark-adapted (scotopic) and light-adapted (photopic) responses to brief flashes at a series of higher intensities were recorded, along with long flashes and random modulations of light levels under photopic conditions.
resultsNegative scotopic threshold responses (nSTRs) had lower amplitudes in rd8 mice compared to WTs. Positive scotopic threshold responses were similar in the two groups. With the more intense stimuli, a- and c-wave amplitudes were smaller in rd8 mice. Both scotopic and photopic b-wave amplitudes tended to be larger in rd8 mice, though generally not significantly.
conclusionsThe striking decrease in nSTR amplitudes was surprising, given that the main retinal effects of the rd8 mutation occur in the outer retina, at the external limiting membrane. The primary source of nSTRs in mice is thought to be at the amacrine cell level in the inner retina. Investigation of how this mutation leads to inner retinal dysfunction might reveal unexpected aspects of retinal cell biology and circuitry.
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