ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Regulation of the on bipolar cell mGluR6 pathway by Ca2+.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 71 citations in OpenAlex.
- Retinoic Acid-Dependent Loss of Synaptic Output from Bipolar Cells Impairs Visual Information Processing in Inherited Retinal Degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Light Adaptation of Retinal Rod Bipolar Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Dopamine D1 and D4 receptors contribute to light adaptation in ON-sustained retinal ganglion cells.Journal of neurophysiology · 2021Article
- A group I metabotropic glutamate receptor controls synaptic gain between rods and rod bipolar cells in the mouse retina.Physiological reports · 2018Article
- The Transduction Cascade in Retinal ON-Bipolar Cells: Signal Processing and Disease.Annual review of vision science · 2017Review
- The TRPM1 channel in ON-bipolar cells is gated by both the α and the βγ subunits of the G-protein Go.Scientific reports · 2016Article
- The Effect of PKCα on the Light Response of Rod Bipolar Cells in the Mouse Retina.Investigative ophthalmology & visual science · 2015Article
- G-protein-mediated inhibition of the Trp channel TRPM1 requires the Gβγ dimer.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- TRP channel gene expression in the mouse retina.Vision research · 2011Article
- Metabotropic glutamate receptors: from the workbench to the bedside.Neuropharmacology · 2011Review
- PKC{alpha} is essential for the proper activation and termination of rod bipolar cell response.Investigative ophthalmology & visual science · 2010Article
- Coordinated control of sensitivity by two splice variants of Gα(o) in retinal ON bipolar cells.The Journal of general physiology · 2010Article
- RGS7 and -11 complexes accelerate the ON-bipolar cell light response.Investigative ophthalmology & visual science · 2010Article
- A transient receptor potential-like channel mediates synaptic transmission in rod bipolar cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Virtual Retina: a biological retina model and simulator, with contrast gain control.Journal of computational neuroscience · 2009Article
- Regulation of ON bipolar cell activity.Progress in retinal and eye research · 2008Review
- Efficiency of synaptic transmission of single-photon events from rod photoreceptor to rod bipolar dendrite.Biophysical journal · 2006Article
- Calcium channel and glutamate receptor activities regulate actin organization in salamander retinal neurons.The Journal of physiology · 2006Article
- Histamine receptors in mammalian retinas.The Journal of comparative neurology · 2006Article
- Modulation by brain natriuretic peptide of GABA receptors on rat retinal ON-type bipolar cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Glutamate produces a hyperpolarizing synaptic potential in On bipolar cells by binding to the metabotropic glutamate receptor mGluR6, leading to closure of a cation channel. Here it is demonstrated that this cation channel is regulated by intracellular Ca(2+). Glutamate-evoked currents were recorded from On bipolar cells in light-adapted salamander retinal slices in the presence of 2 mm external Ca(2+). When glutamate was applied almost continuously, interrupted only briefly to measure the size of the response, the glutamate response remained robust. However, currents elicited by intermittent and brief applications of glutamate exhibited time-dependent run down. Run down of the glutamate response was also voltage dependent, because it was accelerated by membrane hyperpolarization. Run down was triggered, at least in part, by a rise in intracellular Ca(2+); measured as a function of time or voltage, it was attenuated by intracellular buffering of Ca(2+) with BAPTA or by omitting Ca(2+) from the bathing solution. Current-voltage measurements demonstrated that Ca(2+) induced run down of the glutamate response by downregulating cation channel function, rather than by preventing closure of the channel by glutamate and mGluR6. A major source of the Ca(2+) that mediated this inhibition is the cation channel itself, which was found to be permeable to Ca(2+), accounting for the use dependence of the run down. These results suggest that Ca(2+) influx through the cation channel during background illumination could provide a signal to close the cation channel and repolarize the membrane toward its dark potential, an adaptive mechanism for coping with changes in ambient light.
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Identifiers
10844016PMC6772459W1501901319What OpenQuestion holds
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.