ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Regulation of hippocampal synaptic strength by glial xCT.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Sulfur-Containing Amino Acid Homeostasis in the Central Nervous System: From Physiology Regulation to Metal-Induced Neurotoxicity.Metabolites · 2026Review
- Metabolic Regulatory Networks in Ferroptosis During Alzheimer's Disease, Mechanisms of Glial Cell Action, and Pathological Correlations with Neuritic Plaques.International journal of general medicine · 2026Review
- Astrocyte-derived PTN alleviates deficits in hippocampal neurogenesis and cognition in models of multiple sclerosis.Stem cell reports · 2025Article
- Astrocytic HIV-1 Nef Expression Decreases Glutamate Transporter Expression in the Nucleus Accumbens and Increases Cocaine-Seeking Behavior in Rats.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Interference with glutamate antiporter system xExperimental physiology · 2024Article
- Reproducible supervised learning-assisted classification of spontaneous synaptic waveforms with Eventer.Frontiers in neuroinformatics · 2024Article
- Critical Roles of the Cysteine-Glutathione Axis in the Production of γ-Glutamyl Peptides in the Nervous System.International journal of molecular sciences · 2023Review
- Genetic Disruption of System xc-Mediated Glutamate Release from Astrocytes Increases Negative-Outcome Behaviors While Preserving Basic Brain Function in Rat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Tonic extracellular glutamate and ischaemia: glutamate antiporter system xThe Journal of physiology · 2023Article
- Sex- and age-dependent contribution of System xFrontiers in behavioral neuroscience · 2023Article
- Lifespan extension with preservation of hippocampal function in aged system xMolecular psychiatry · 2022Article
- Hyperexcitability and brain morphological differences in mice lacking the cystine/glutamate antiporter, system xJournal of neuroscience research · 2021Article
- Corticostriatal dysfunction and social interaction deficits in mice lacking the cystine/glutamate antiporter.Molecular psychiatry · 2021Article
- Influence of glutamate and GABA transport on brain excitatory/inhibitory balance.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Glutamate homeostasis and dopamine signaling: Implications for psychostimulant addiction behavior.Neurochemistry international · 2021Review
- Neuronal hibernation following hippocampal demyelination.Acta neuropathologica communications · 2021Article
- Validation of a System xFrontiers in cellular neuroscience · 2021Article
- Aged xCT-Deficient Mice Are Less Susceptible for Lactacystin-, but Not 1-Methyl-4-Phenyl-1,2,3,6- Tetrahydropyridine-, Induced Degeneration of the Nigrostriatal Pathway.Frontiers in cellular neuroscience · 2021Article
- Identification, Expression, and Roles of the Cystine/Glutamate Antiporter in Ocular Tissues.Oxidative medicine and cellular longevity · 2020Review
- Neurotransmitter changes after traumatic brain injury: an update for new treatment strategies.Molecular psychiatry · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most extracellular glutamate in the brain is released by xCT, a glial antiporter that exports glutamate and imports cystine. The function of xCT, and extracellular glutamate in general, remains unclear. Several lines of evidence suggest that glutamate from xCT could act in a paracrine fashion to suppress glutamatergic synapse strength by triggering removal of postsynaptic glutamate receptors. To test this idea, we used whole-cell patch-clamp electrophysiology and immunohistochemistry to quantify receptor number and synapse function in xCT knock-out mouse hippocampal CA3-CA1 synapses. Consistent with the hypothesis that xCT suppresses glutamate receptor number and synapse strength, xCT knock-out synapses showed increased AMPA receptor abundance with concomitant large enhancements of spontaneous and evoked synaptic transmission. We saw no evidence for changes in GABA receptor abundance or the overall number of glutamatergic synapses. The xCT knock-out phenotype was replicated by incubating slices in the xCT inhibitor (S)-4-carboxyphenylglycine, and consistent with the idea that xCT works by regulating extracellular glutamate, the xCT knock-out phenotype could be reproduced in controls by incubating the slices in glutamate-free aCSF. We conclude that glutamate secreted via xCT suppresses glutamatergic synapse strength by triggering removal of postsynaptic AMPA 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.