ArticleJournal of neurophysiology2012
Synaptic pathways that shape the excitatory drive in an OFF retinal ganglion cell.
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 33 papers.
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Who cites it
33 citing papers in PubMed, 41 citations in OpenAlex.
- Inhibitory Circuits Can Restore OFF Pathway Responses in Retinal Prostheses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Correlation of contrast sensitivity at low spatial frequencies with myopic shift in Chinese children.BMC ophthalmology · 2025Article
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- Cellular Characterization and Interspecies Evolution of the Tree Shrew Retina across Postnatal Lifespan.Research (Washington, D.C.) · 2024Article
- Calcium-permeable AMPA receptors on AII amacrine cells mediate sustained signaling in the On-pathway of the primate retina.Cell reports · 2022Article
- Essential Roles of Tbr1 in the Formation and Maintenance of the Orientation-Selective J-RGCs and a Group of OFF-Sustained RGCs in Mouse.Cell reports · 2019Article
- Extrasynaptic NMDA Receptors on Rod Pathway Amacrine Cells: Molecular Composition, Activation, and Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Selective synaptic connections in the retinal pathway for night vision.The Journal of comparative neurology · 2019Article
- Directional excitatory input to direction-selective ganglion cells in the rabbit retina.The Journal of comparative neurology · 2019Article
- Extract of the Blood Circulation-Promoting Recipe-84 Can Protect Rat Retinas by Inhibiting the β-Catenin Signaling Pathway.International journal of molecular sciences · 2018Article
- Article
- Article
- Synaptic Mechanisms Generating Orientation Selectivity in the ON Pathway of the Rabbit Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Functional Circuitry of the Retina.Annual review of vision science · 2015Article
- APLP2 Regulates Refractive Error and Myopia Development in Mice and Humans.PLoS genetics · 2015Article
- Inhibitory input to the direction-selective ganglion cell is saturated at low contrast.Journal of neurophysiology · 2015Article
- Function and Circuitry of VIP+ Interneurons in the Mouse Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Alterations in Kainate Receptor and TRPM1 Localization in Bipolar Cells after Retinal Photoreceptor Degeneration.Frontiers in cellular neuroscience · 2015Article
- Properties of a Glutamatergic Synapse Controlling Information Output from Retinal Bipolar Cells.PloS one · 2015Article
- Adeno-associated virus-RNAi of GlyRα1 and characterization of its synapse-specific inhibition in OFF alpha transient retinal ganglion cells.Journal of neurophysiology · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Different types of retinal ganglion cells represent distinct spatiotemporal filters that respond selectively to specific features in the visual input. Much about the circuitry and synaptic mechanisms that underlie such specificity remains to be determined. This study examines how N-methyl-d-aspartate (NMDA) receptor signaling combines with other excitatory and inhibitory mechanisms to shape the output of small-field OFF brisk-sustained ganglion cells (OFF-BSGCs) in the rabbit retina. We used voltage clamp to separately resolve NMDA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and inhibitory inputs elicited by stimulation of the receptive field center. Three converging circuits were identified. First is a direct glutamatergic input, arising from OFF cone bipolar cells (CBCs), which is mediated by synaptic NMDA and AMPA receptors. The NMDA input was saturated at 10% contrast, whereas the AMPA input increased monotonically up to 60% contrast. We propose that NMDA inputs selectively enhance sensitivity to low contrasts. The OFF bipolar cells, mediating this direct excitatory input, express dendritic kainate (KA) receptors, which are resistant to the nonselective AMPA/KA receptor antagonist, 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide disodium salt (NBQX), but are suppressed by a GluK1- and GluK3-selective antagonist, (S)-1-(2-amino-2-carboxyethyl)-3-(2-carboxy-thiophene-3-yl-methyl)-5-methylpyrimidine-2,4-dione (UBP-310). The second circuit entails glycinergic crossover inhibition, arising from ON-CBCs and mediated by AII amacrine cells, which modulate glutamate release from the OFF-CBC terminals. The third circuit also comprises glycinergic crossover inhibition, which is driven by the ON pathway; however, this inhibition impinges directly on the OFF-BSGCs and is mediated by an unknown glycinergic amacrine cell that expresses AMPA but not KA receptors.
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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.