ArticleJournal of neurophysiology2012
Depolarizing bipolar cell dysfunction due to a Trpm1 point mutation.
Article in Journal of neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
The trial behind it
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
36 citing papers in PubMed, 48 citations in OpenAlex.
- Upregulated TRPM1 is associated with apoptosis in Rs1 knockout mice and in ARPE19 cells through increased intracellular calcium.Scientific reports · 2026Article
- Increased sensitivity to myopia and altered retinal ON/OFF balance in a mouse model lackingbioRxiv : the preprint server for biology · 2025Article
- Identifying genetic determinants of outer retinal function in mice using a large-scale gene-targeted screen.PLoS genetics · 2025Article
- Gene therapy shines light on congenital stationary night blindness for future cures.Journal of translational medicine · 2025Review
- Review
- Loss of ON-Pathway Function in Mice Lacking Lrit3 Decreases Recovery From Lens-Induced Myopia.Investigative ophthalmology & visual science · 2024Article
- Mice LackingInternational journal of molecular sciences · 2022Article
- A New Mouse Model for Complete Congenital Stationary Night Blindness Due toInternational journal of molecular sciences · 2021Article
- Molecular mechanisms underlying selective synapse formation of vertebrate retinal photoreceptor cells.Cellular and molecular life sciences : CMLS · 2020Review
- TRPM3_miR-204: a complex locus for eye development and disease.Human genomics · 2020Review
- Reduced expression of theMolecular vision · 2019Article
- Phenotypic characterization of complete CSNB in the inbred research beagle: how common is CSNB in research and companion dogs?Documenta ophthalmologica. Advances in ophthalmology · 2018Article
- The TRPM1 Channel Is Required for Development of the Rod ON Bipolar Cell-AII Amacrine Cell Pathway in the Retinal Circuit.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- The Transduction Cascade in Retinal ON-Bipolar Cells: Signal Processing and Disease.Annual review of vision science · 2017Review
- A missense mutation inJournal of neurophysiology · 2017Article
- LRIT3 Differentially Affects Connectivity and Synaptic Transmission of Cones to ON- and OFF-Bipolar Cells.Investigative ophthalmology & visual science · 2017Article
- A mutagenesis-derivedMolecular vision · 2017Article
- Article
- A Chemical Mutagenesis Screen Identifies Mouse Models with ERG Defects.Advances in experimental medicine and biology · 2016Article
- Intravitreal delivery of a novel AAV vector targets ON bipolar cells and restores visual function in a mouse model of complete congenital stationary night blindness.Human molecular genetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
Mutations in TRPM1 are found in humans with an autosomal recessive form of complete congenital stationary night blindness (cCSNB). The Trpm1(-/-) mouse has been an important animal model for this condition. Here we report a new mouse mutant, tvrm27, identified in a chemical mutagenesis screen. Genetic mapping of the no b-wave electroretinogram (ERG) phenotype of tvrm27 localized the mutation to a chromosomal region that included Trpm1. Complementation testing with Trpm1(-/-) mice confirmed a mutation in Trpm1. Sequencing identified a nucleotide change in exon 23, converting a highly conserved alanine within the pore domain to threonine (p.A1068T). Consistent with prior studies of Trpm1(-/-) mice, no anatomical changes were noted in the Trpm1(tvrm27/tvrm27) retina. The Trpm1(tvrm27/tvrm27) phenotype is distinguished from that of Trpm1(-/-) by the retention of TRPM1 expression on the dendritic tips of depolarizing bipolar cells (DBCs). While ERG b-wave amplitudes of Trpm1(+/-) heterozygotes are comparable to wild type, those of Trpm1(+/tvrm27) mice are reduced by 32%. A similar reduction in the response of Trpm1(+/tvrm27) DBCs to LY341495 or capsaicin is evident in whole cell recordings. These data indicate that the p.A1068T mutant TRPM1 acts as a dominant negative with respect to TRPM1 channel function. Furthermore, these data indicate that the number of functional TRPM1 channels at the DBC dendritic tips is a key factor in defining DBC response amplitude. The Trpm1(tvrm27/tvrm27) mutant will be useful for elucidating the role of TRPM1 in DBC signal transduction, for determining how Trpm1 mutations impact central visual processing, and for evaluating experimental therapies for cCSNB.
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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.