ArticleJournal of neurophysiology2012
mGluR6 deletion renders the TRPM1 channel in retina inactive.
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 45 papers.
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Who cites it
45 citing papers in PubMed, 75 citations in OpenAlex.
- Structural basis for modulation of group III mGlu receptors by transsynaptic interactions.Science advances · 2026Article
- Upregulated TRPM1 is associated with apoptosis in Rs1 knockout mice and in ARPE19 cells through increased intracellular calcium.Scientific reports · 2026Article
- Cryo-EM structure of TRPM1 reveals a non-canonical architecture with an inverted transmembrane domain.Nature communications · 2026Article
- The Retinal Light Response Is Modulated by an mGluR5-Mediated Retrograde Signal from ON-Bipolar Cells to Photoreceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- The retinal light response is modulated by an mGluR5-mediated retrograde signal from ON-bipolar cells to photoreceptors.bioRxiv : the preprint server for biology · 2025Article
- A mechanism for pathological oscillations in mouse retinal ganglion cells in a model of night blindness.The Journal of general physiology · 2025Article
- Trans-synaptic Interaction with mGluR6 Contributes to ELFN1 Presynaptic Enrichment in Rod Photoreceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Divergent mechanisms of neural adaptation and instability in the mammalian retina.Current biology : CB · 2025Article
- Interaction between native and prosthetic visual responses in optogenetic visual restoration.JCI insight · 2025Article
- Review
- AInternational journal of molecular sciences · 2024Article
- The odyssey of the TR(i)P journey to the cellular membrane.Frontiers in cell and developmental biology · 2024Review
- Selective Block of Upregulated Kv1.3 Potassium Channels in ON-Bipolar Cells of the Blind Retina Enhances Optogenetically Restored Signaling.International journal of molecular sciences · 2023Article
- Trophoblast glycoprotein is required for efficient synaptic vesicle exocytosis from retinal rod bipolar cells.Frontiers in cellular neuroscience · 2023Article
- Bipolar cell targeted optogenetic gene therapy restores parallel retinal signaling and high-level vision in the degenerated retina.Communications biology · 2022Article
- Divergent outer retinal circuits drive image and non-image visual behaviors.Cell reports · 2022Article
- Development and maintenance of vision's first synapse.Developmental biology · 2021Review
- Mice with mutations in Trpm1, a gene in the locus of 15q13.3 microdeletion syndrome, display pronounced hyperactivity and decreased anxiety-like behavior.Molecular brain · 2021Article
- Restoration of mGluR6 Localization Following AAV-Mediated Delivery in a Mouse Model of Congenital Stationary Night Blindness.Investigative ophthalmology & visual science · 2021Article
- Two Functional Classes of Rod Bipolar Cells in the Healthy and Degenerated Optogenetically Treated Murine Retina.Frontiers in cellular neuroscience · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 4 countries.
Funding
Abstract
In darkness, glutamate released from photoreceptors activates the metabotropic glutamate receptor 6 (mGluR6) on retinal ON bipolar cells. This activates the G protein G(o), which then closes transient receptor potential melastatin 1 (TRPM1) channels, leading to cells' hyperpolarization. It has been generally assumed that deleting mGluR6 would render the cascade inactive and the ON bipolar cells constitutively depolarized. Here we show that the rod bipolar cells in mGluR6-null mice were hyperpolarized. The slope conductance of the current-voltage curves and the current noise were smaller than in wild type. Furthermore, while in wild-type rod bipolar cells, TRPM1 could be activated by local application of capsaicin; in null cells, it did not. These results suggest that the TRPM1 channel in mGluR6-null rod bipolar cells is inactive. To explore the reason for this lack of activity, we tested if mGluR6 deletion affected expression of cascade components. Immunostaining for G protein subunit candidates Gα(o), Gβ(3), and Gγ(13) showed no significant changes in their expression or distribution. Immunostaining for TRPM1 in the dendritic tips was greatly reduced, but the channel was still present in the soma and primary dendrites of mGluR6-null bipolar cells, where a certain fraction of TRPM1 appears to localize to the plasma membrane. Consequently, the lack of TRPM1 activity in the null retina is unlikely to be due to failure of the channels to localize to the plasma membrane. We speculate that, to be constitutively active, TRPM1 channels in ON bipolar cells have to be in a complex, or perhaps require an unidentified factor.
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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.