ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
Deletion of Neuronal GLT-1 in Mice Reveals Its Role in Synaptic Glutamate Homeostasis and Mitochondrial Function.
Erratum issuedOpen access · bronzeAbstract read
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Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.
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37citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
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Who cites it
37 citing papers in PubMed, 60 citations in OpenAlex.
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- Misprogramming of glucose metabolism impairs recovery of hippocampal slices from neuronal GLT-1 knockout mice and contributes to excitotoxic injury through mitochondrial superoxide production.Journal of neurochemistry · 2025Article
- PS1/gamma-secretase acts as rogue chaperone of glutamate transporter EAAT2/GLT-1 in Alzheimer's disease.Acta neuropathologica communications · 2024Article
- Pathological Interplay between Inflammation and Mitochondria Aggravates Glutamate Toxicity.International journal of molecular sciences · 2024Review
- PS1/gamma-secretase acts as rogue chaperone of glutamate transporter EAAT2/GLT-1 in Alzheimer's disease.Research square · 2023Article
- Inhibition of mGluR5 alters BDNF/TrkB and GLT-1 expression in the prefrontal cortex and hippocampus and ameliorates PTSD-like behavior in rats.Psychopharmacology · 2023Article
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- Asymmetric dysregulation of glutamate dynamics across the synaptic cleft in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
20 authors at 3 institutions in 3 countries.
Laura F McNairDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.ORCID 0000-0002-5213-9931
Jens V AndersenDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.ORCID 0000-0001-8767-2675
Blanca I AldanaDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.
Michaela C HohnholtDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.
Jakob D NissenDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.
Yan SunDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Kathryn D FischerDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Ursula SonnewaldDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.
Nils NybergDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.
Sophie C WebsterDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Kush KapurDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Theresa S RimmeleDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Ilaria BaroneDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Hannah Hawks-MayerDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Jonathan O LiptonDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Nathaniel W HodgsonDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.ORCID 0000-0001-8299-3963
Takao K HenschDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115.
Chiye J AokiCenter of Neural Science, New York University, New York, New York 10003.ORCID 0000-0003-4010-9425
Paul A RosenbergDepartment of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts 02115, helle.waagepetersen@sund.ku.dk paul.rosenberg@childrens.harvard.edu.ORCID 0000-0002-5185-1118
Helle S WaagepetersenDepartment of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark, helle.waagepetersen@sund.ku.dk paul.rosenberg@childrens.harvard.edu.ORCID 0000-0003-4583-8379
Boston Children's Hospital · USUniversity of Copenhagen · DKNYU Langone Health · US
Funding
SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2MVision Core Grant- Design and Fabrication ModuleP30EY013079 · NEI · NEW YORK UNIVERSITY · PI MOVSHON, J ANTHONY · 2000 to 2025
$14.2MSupplement request for Training GrantT32NS007473 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI Elizabeth C. Engle, Thomas L. Schwarz · 1999 to 2026
$6.9MMouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI SAHIN, MUSTAFA · 2016 to 2020
$5.2MZinc is a critical regulator of cell death and axon regeneration after CNS injuryR01EY024481 · NEI · BOSTON CHILDREN'S HOSPITAL · PI BENOWITZ, LARRY IRA, ROSENBERG, PAUL ALLEN · 2015 to 2019
$2.8MThe Role of Cell-Type Specific Expression of GLT1 at Excitatory SynapsesR01NS066019 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI ROSENBERG, PAUL ALLEN · 2010 to 2014
$2.8MNeuronal regulation of glutamate homeostasis R21MH104318 · NIMH · BOSTON CHILDREN'S HOSPITAL · PI ROSENBERG, PAUL ALLEN · 2015 to 2016
$498kTo eat or run? The role of GABA in the hippocampus-prefrontal cortex circuit for decision makingR21MH105846 · NIMH · NEW YORK UNIVERSITY · PI AOKI, CHIYE J · 2014 to 2015
$417kNEI NIH HHS P30 EY013079NEI NIH HHS R01 EY024481NICHD NIH HHS P30 HD018655NICHD NIH HHS U54 HD090255NIMH NIH HHS R21 MH104318NIMH NIH HHS R21 MH105846NINDS NIH HHS R01 NS066019NINDS NIH HHS T32 NS007473
Abstract
The glutamate transporter GLT-1 is highly expressed in astrocytes but also in neurons, primarily in axon terminals. We generated a conditional neuronal GLT-1 KO using synapsin 1-Cre (synGLT-1 KO) to elucidate the metabolic functions of GLT-1 expressed in neurons, here focusing on the cerebral cortex. Both synaptosomal uptake studies and electron microscopic immunocytochemistry demonstrated knockdown of GLT-1 in the cerebral cortex in the synGLT-1 KO mice. Aspartate content was significantly reduced in cerebral cortical extracts as well as synaptosomes from cerebral cortex of synGLT-1 KO compared with control littermates.
Indexed as
AnimalsAspartic AcidCerebral CortexExcitatory Amino Acid Transporter 2Glutamic AcidHomeostasisMiceMice, KnockoutMitochondriaNeuronsOxygen ConsumptionPresynaptic TerminalsSynapsesSynaptosomesAspartic AcidExcitatory Amino Acid Transporter 2Glutamic AcidSlc1a2 protein, mouseanaplerosisaspartatebioenergeticsHuntington'sneurodegenerationTCA cycle
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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.