ArticleThe Journal of physiology2011
GluA4 is indispensable for driving fast neurotransmission across a high-fidelity central synapse.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 63 citations in OpenAlex.
- Tunable AMPA receptor function via recurrent evolution of heterotetramers.The Journal of general physiology · 2026Article
- Synaptic Facilitation Enhances the Reliability and Precision of High-Frequency Neurotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Structural basis for activation and conformational plasticity of the GluA4 AMPA receptor.Nature communications · 2026Article
- Input-Specific Organization of Intrinsic Excitability Expands Coding Capacity of Fast-Spiking Auditory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- GluA4 AMPA receptor gating mechanisms and modulation by auxiliary proteins.Nature structural & molecular biology · 2025Article
- Intersectin-1 enhances calcium-dependent replenishment of the readily releasable pool of synaptic vesicles during development.The Journal of physiology · 2025Article
- AMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases.Cellular and molecular neurobiology · 2025Review
- Cellular and synaptic specializations for sub-millisecond precision in the mammalian auditory brainstem.Frontiers in cellular neuroscience · 2025Review
- Fxr1 Deletion from Cortical Parvalbumin Interneurons Modifies Their Excitatory Synaptic Responses.eNeuro · 2025Article
- Fusion pore flux controls the rise-times of quantal synaptic responses.The Journal of general physiology · 2024Article
- Molecular and functional profiling of cell diversity and identity in the lateral superior olive, an auditory brainstem center with ascending and descending projections.Frontiers in cellular neuroscience · 2024Article
- Inter and intralaminar excitation of parvalbumin interneurons in mouse barrel cortex.PloS one · 2024Article
- Maintenance of a central high frequency synapse in the absence of synaptic activity.Frontiers in cellular neuroscience · 2024Article
- AMPAR receptor inhibitors suppress proliferation of human small cell lung cancer cell lines.Thoracic cancer · 2023Article
- Inter and Intralaminar Excitation of Parvalbumin Interneurons in Mouse Barrel Cortex.bioRxiv : the preprint server for biology · 2023Article
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- Neuroligin-3 confines AMPA receptors into nanoclusters, thereby controlling synaptic strength at the calyx of Held synapses.Science advances · 2022Article
- Article
- Role of GluA4 in the acoustic and tactile startle responses.Hearing research · 2022Article
- Loss of miR-183/96 Alters Synaptic Strength via Presynaptic and Postsynaptic Mechanisms at a Central Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Fast excitatory synaptic transmission in central synapses is mediated primarily by AMPA receptors (AMPARs), which are heteromeric assemblies of four subunits, GluA1-4. Among these subunits, rapidly gating GluA3/4 appears to be the most abundantly expressed to enable neurotransmission with submillisecond precision at fast rates in subsets of central synapses. However, neither definitive identification of the molecular substrate for native AMPARs in these neurons, nor their hypothesized functional roles in vivo has been unequivocally demonstrated, largely due to lack of specific antagonists. Using GluA3 or GluA4 knockout (KO) mice, we investigated these issues at the calyx of Held synapse, which is known as a high-fidelity synapse involved in sound localization. Patch-clamp recordings from postsynaptic neurons showed that deletion of GluA4 significantly slowed the time course of both evoked and miniature AMPAR-mediated excitatory postsynaptic currents (AMPAR-EPSCs), reduced their amplitude, and exacerbated AMPAR desensitization and short-term depression (STD). Surprisingly, presynaptic release probability was also elevated, contributing to severe STD at GluA4-KO synapses. In contrast, only marginal changes in AMPAR-EPSCs were found in GluA3-KO mice. Furthermore, independent of changes in intrinsic excitability of postsynaptic neurons, deletion of GluA4 markedly reduced synaptic drive and increased action potential failures during high-frequency activity, leading to profound deficits in specific components of the auditory brainstem responses associated with synchronized spiking in the calyx of Held synapse and other related neurons in vivo. These observations identify GluA4 as the main determinant for fast synaptic response, indispensable for driving high-fidelity neurotransmission and conveying precise temporal information.
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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.