ArticleChannels (Austin, Tex.)2015
Gain-of-function nature of Cav1.4 L-type calcium channels alters firing properties of mouse retinal ganglion cells.
Article in Channels (Austin, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Exploring the potential for gene therapy in Cav1.4-related retinal channelopathies.Channels (Austin, Tex.) · 2025Review
- Quantitative Proteomics Identifies Potential Molecular Adaptations in Mouse Models of Congenital Stationary Night Blindness Type 2.Molecular & cellular proteomics : MCP · 2025Article
- Calcium Channels in Retinal Function and Disease.Annual review of vision science · 2022Review
- Cav1.4 dysfunction and congenital stationary night blindness type 2.Pflugers Archiv : European journal of physiology · 2021Review
- Knockout of CaScientific reports · 2021Article
- Function of cone and cone-related pathways in CaScientific reports · 2021Article
- Functional impact of a congenital stationary night blindness type 2 mutation depends on subunit composition of CaThe Journal of biological chemistry · 2020Article
- Transgenic Expression ofTranslational vision science & technology · 2020Article
- Article
- L-type voltage-gated calcium channels in stem cells and tissue engineering.Cell proliferation · 2019Review
- Disinhibition of intrinsic photosensitive retinal ganglion cells in patients with X-linked congenital stationary night blindness.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
- Photoreceptor degeneration in a new Cacna1f mutant mouse model.Experimental eye research · 2019Article
- Voltage-Gated Calcium Channels: Key Players in Sensory Coding in the Retina and the Inner Ear.Physiological reviews · 2018Review
- αThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Relevance of tissue specific subunit expression in channelopathies.Neuropharmacology · 2018Review
- Channeling Vision: CaBioMed research international · 2018Review
- Cone dystrophy and ectopic synaptogenesis in a Cacna1f loss of function model of congenital stationary night blindness (CSNB2A).Channels (Austin, Tex.) · 2018Article
- LRIT3 Differentially Affects Connectivity and Synaptic Transmission of Cones to ON- and OFF-Bipolar Cells.Investigative ophthalmology & visual science · 2017Article
- Degrading vision with too much Ca(2+).Channels (Austin, Tex.) · 2015Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Proper function of Cav1.4 L-type calcium channels is crucial for neurotransmitter release in the retina. Our understanding about how different levels of Cav1.4 channel activity affect retinal function is still limited. In the gain-of-function mouse model Cav1.4-IT we expected a reduction in the photoreceptor dynamic range but still transmission toward retinal ganglion cells. A fraction of Cav1.4-IT ganglion cells responded to light stimulation in multielectrode array recordings from whole-mounted retinas, but showed a significantly delayed response onset. Another significant number of cells showed higher activity in darkness. In addition to structural remodeling observed at the first retinal synapse of Cav1.4-IT mice the functional data suggested a loss of contrast enhancement, a fundamental feature of our visual system. In fact, Cav1.4-IT mouse retinas showed a decline in spatial response and changes in their contrast sensitivity profile. Photoreceptor degeneration was obvious from the nodular structure of cone axons and enlarged pedicles which partly moved toward the outer nuclear layer. Loss of photoreceptors was also expressed as reduced expression of proteins involved in chemical and electrical transmission, as such metabotropic glutamate receptor mGluR6 and the gap junction protein Connexin 36. Such gross changes in retinal structure and function could also explain the diminished visual performance of CSNB2 patients. The expression pattern of the plasma-membrane calcium ATPase 1 which participates in the maintenance of the intracellular calcium homeostasis in photoreceptors was changed in Cav1.4-IT mice. This might be part of a protection mechanism against increased calcium influx, as this is suggested for Cav1.4-IT channels.
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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.