ArticleBiophysical journal2011
The discovery of slowness: low-capacity transport and slow anion channel gating by the glutamate transporter EAAT5.
Article in Biophysical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Excitatory Amino Acid Transporters as Therapeutic Targets in the Treatment of Neurological Disorders: Their Roles and Therapeutic Prospects.Neurochemical research · 2025Review
- Glutamate transporters are involved in direct inhibitory synaptic transmission in the vertebrate retina.Open biology · 2024Article
- EAAT5 glutamate transporter rapidly binds glutamate with micromolar affinity in mouse rods.The Journal of general physiology · 2023Article
- Mechanisms of simultaneous linear and nonlinear computations at the mammalian cone photoreceptor synapse.Nature communications · 2023Article
- Mutation in glutamate transporter homologue GltTk provides insights into pathologic mechanism of episodic ataxia 6.Nature communications · 2023Article
- Functional and Kinetic Comparison of Alanine Cysteine Serine Transporters ASCT1 and ASCT2.Biomolecules · 2022Article
- Reconstitution of GABA, Glycine and Glutamate Transporters.Neurochemical research · 2022Review
- Molecular Basis of Coupled Transport and Anion Conduction in Excitatory Amino Acid Transporters.Neurochemical research · 2022Review
- Rapid Regulation of Glutamate Transport: Where Do We Go from Here?Neurochemical research · 2022Review
- Influence of glutamate and GABA transport on brain excitatory/inhibitory balance.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- EAAT5 Glutamate Transporter-Mediated Inhibition in the Vertebrate Retina.Frontiers in cellular neuroscience · 2021Review
- EAAT2 Expression in the Hippocampus, Subiculum, Entorhinal Cortex and Superior Temporal Gyrus in Alzheimer's Disease.Frontiers in cellular neuroscience · 2021Article
- Cellular Physiology and Pathophysiology of EAAT Anion Channels.Frontiers in cellular neuroscience · 2021Review
- The Regulation of Astrocytic Glutamate Transporters in Health and Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Resting and stimulated mouse rod photoreceptors show distinct patterns of vesicle release at ribbon synapses.The Journal of general physiology · 2020Article
- An amino-terminal point mutation increases EAAT2 anion currents without affecting glutamate transport rates.The Journal of biological chemistry · 2020Article
- Excitatory Amino Acid Transporters (EAATs): Glutamate Transport and Beyond.International journal of molecular sciences · 2019Review
- Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System.International journal of molecular sciences · 2019Review
- The role of glutamate transporters in the pathophysiology of neuropsychiatric disorders.NPJ schizophrenia · 2017Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Excitatory amino acid transporters (EAATs) control the glutamate concentration in the synaptic cleft by glial and neuronal glutamate uptake. Uphill glutamate transport is achieved by the co-/countertransport of Na(+) and other ions down their concentration gradients. Glutamate transporters also display an anion conductance that is activated by the binding of Na(+) and glutamate but is not thermodynamically coupled to the transport process. Of the five known glutamate transporter subtypes, the retina-specific subtype EAAT5 has the largest conductance relative to glutamate uptake activity. Our results suggest that EAAT5 behaves as a slow-gated anion channel with little glutamate transport activity. At steady state, EAAT5 was activated by glutamate, with a K(m)= 61 ± 11 μM. Binding of Na(+) to the empty transporter is associated with a K(m) = 229 ± 37 mM, and binding to the glutamate-bound form is associated with a K(m) = 76 ± 40 mM. Using laser-pulse photolysis of caged glutamate, we determined the pre-steady-state kinetics of the glutamate-induced anion current of EAAT5. This was characterized by two exponential components with time constants of 30 ± 1 ms and 200 ± 15 ms, which is an order of magnitude slower than those observed in other glutamate transporters. A voltage-jump analysis of the anion currents indicates that the slow activation behavior is caused by two slow, rate-limiting steps in the transport cycle, Na(+) binding to the empty transporter, and translocation of the fully loaded transporter. We propose a kinetic transport scheme that includes these two slow steps and can account for the experimentally observed data. Overall, our results suggest that EAAT5 may not act as a classical high-capacity glutamate transporter in the retina; rather, it may function as a slow-gated glutamate receptor and/or glutamate buffering system.
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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.