ArticleNature communications2015
Synaptic GABA release prevents GABA transporter type-1 reversal during excessive network activity.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- GABA transporter 1 is a promising drug target for CUL4B mutation-associated epilepsy.Acta pharmacologica Sinica · 2025Article
- Insomnia treatment based on the regulation of the GABAergic system: traditional Chinese medicine perspectives and therapeutic approaches.Frontiers in neuroscience · 2025Review
- Expression of GAD2 in excitatory neurons projecting from the ventrolateral periaqueductal gray to the locus coeruleus.iScience · 2024Article
- Dynamical changes in the expression of GABAergic and purinergic components occur during the polarization of THP-1 monocytes to proinflammatory macrophages.Biochemistry and biophysics reports · 2023Article
- Circadian rhythm disruptions associated with opioid use disorder in synaptic proteomes of human dorsolateral prefrontal cortex and nucleus accumbens.Molecular psychiatry · 2023Article
- GABA tone regulation and its cognitive functions in the brain.Nature reviews. Neuroscience · 2023Review
- Volume-transmitted GABA waves pace epileptiform rhythms in the hippocampal network.Current biology : CB · 2023Article
- GABA Release from Astrocytes in Health and Disease.International journal of molecular sciences · 2022Review
- Oligodendroglial GABAergic Signaling: More Than Inhibition!Neuroscience bulletin · 2021Review
- Spontaneous CaFrontiers in cellular neuroscience · 2021Article
- Environmental enrichment implies GAT-1 as a potential therapeutic target for stroke recovery.Theranostics · 2021Article
- Molecular Dynamic Simulations to Probe Stereoselectivity of Tiagabine Binding with Human GAT1.Molecules (Basel, Switzerland) · 2020Article
- A Reappraisal of GAT-1 Localization in Neocortex.Frontiers in cellular neuroscience · 2020Review
- The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs.Oxidative medicine and cellular longevity · 2019Review
- Modeling and Simulation ofComputational and structural biotechnology journal · 2019Article
- Modulation of Neocortical Development by Early Neuronal Activity: Physiology and Pathophysiology.Frontiers in cellular neuroscience · 2017Review
- Astrocytic GABA transporter activity modulates excitatory neurotransmission.Nature communications · 2016Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
GABA transporters control extracellular GABA, which regulates the key aspects of neuronal and network behaviour. A prevailing view is that modest neuronal depolarization results in GABA transporter type-1 (GAT-1) reversal causing non-vesicular GABA release into the extracellular space during intense network activity. This has important implications for GABA uptake-targeting therapies. Here we combined a realistic kinetic model of GAT-1 with experimental measurements of tonic GABAA receptor currents in ex vivo hippocampal slices to examine GAT-1 operation under varying network conditions. Our simulations predict that synaptic GABA release during network activity robustly prevents GAT-1 reversal. We test this in the 0 Mg(2+) model of epileptiform discharges using slices from healthy and chronically epileptic rats and find that epileptiform activity is associated with increased synaptic GABA release and is not accompanied by GAT-1 reversal. We conclude that sustained efflux of GABA through GAT-1 is unlikely to occur during physiological or pathological network activity.
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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.