ArticleHuman molecular genetics2022
Differential impact of Kv8.2 loss on rod and cone signaling and degeneration.
Article in Human molecular genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Kv2.1/Kv8.2 Channels Regulate Fluid Homeostasis in the Outer Retina.bioRxiv : the preprint server for biology · 2026Article
- Loss of Kv8.2 in the Mouse Retina Is Associated With Altered One-Carbon Metabolism.Journal of neurochemistry · 2026Article
- Article
- A Kv2 inhibitor combination reveals native neuronal conductances consistent with Kv2/KvS heteromers.eLife · 2025Article
- Effects of different anesthetic drugs on electroretinography in mice.Scientific reports · 2025Article
- Analysis of the relationship between rod cell membrane currents and the photoreceptor component of electroretinograms using a cable model.Scientific reports · 2025Article
- The Electrically Silent Kv5.1 Subunit Forms Heteromeric Kv2 Channels in Cortical Neurons and Confers Distinct Functional Properties.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Mouse all-cone retina models of Cav1.4 synaptopathy.Frontiers in molecular neuroscience · 2023Article
- The origins of the full-field flash electroretinogram b-wave.Frontiers in molecular neuroscience · 2023Review
- Sex-related differences in retinal function in Wistar rats: implications for toxicity and safety studies.Frontiers in toxicology · 2023Article
- Cone-Driven Retinal Responses Are Shaped by Rod But Not Cone HCN1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Heteromeric Kv2.1/Kv8.2 channels are voltage-gated potassium channels localized to the photoreceptor inner segment. They carry IKx, which is largely responsible for setting the photoreceptor resting membrane potential. Mutations in Kv8.2 result in childhood-onset cone dystrophy with supernormal rod response (CDSRR). We generated a Kv8.2 knockout (KO) mouse and examined retinal signaling and photoreceptor degeneration to gain deeper insight into the complex phenotypes of this disease. Using electroretinograms, we show that there were delayed or reduced signaling from rods depending on the intensity of the light stimulus, consistent with reduced capacity for light-evoked changes in membrane potential. The delayed response was not seen ex vivo where extracellular potassium levels were controlled by the perfusion buffer, so we propose the in vivo alteration is influenced by genotype-associated ionic imbalance. We observed mild retinal degeneration. Signaling from cones was reduced but there was no loss of cone density. Loss of Kv8.2 altered responses to flickering light with responses attenuated at high frequencies and altered in shape at low frequencies. The Kv8.2 KO line on an all-cone retina background had reduced cone-driven ERG b wave amplitudes and underwent degeneration. Altogether, we provide insight into how a deficit in the dark current affects the health and function of photoreceptors.
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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.