ArticleNeuroscience2014
Isoflurane unveils a critical role of glutamate transporter type 3 in regulating hippocampal GluR1 trafficking and context-related learning and memory in mice.
Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The Janus Face of Isoflurane: A Dose-Age-Response Model of Cognitive Impact.Biomolecules · 2026Review
- Modulating AMPA receptor-dependent synaptic plasticity: Mechanistic interventions against remifentanil-induced hyperalgesia in reoperative rats - A randomised controlled trial.Indian journal of anaesthesia · 2025Article
- Cerebral Glutamate Regulation and Receptor Changes in Perioperative Neuroinflammation and Cognitive Dysfunction.Biomolecules · 2022Review
- Article
- A multi-omic analysis of the dorsal striatum in an animal model of divergent genetic risk for alcohol use disorder.Journal of neurochemistry · 2021Article
- Neuronal excitatory amino acid transporter EAAT3: Emerging functions in health and disease.Neurochemistry international · 2019Article
- Exploring the Effect of Endoplasmic Reticulum Stress Inhibition by 4-Phenylbutyric Acid on AMPA-Induced Hippocampal Excitotoxicity in Rat Brain.Neurotoxicity research · 2019Article
- Sevoflurane-induced memory impairment in the postnatal developing mouse brain.Experimental and therapeutic medicine · 2018Article
- Isoflurane promotes glucose metabolism through up-regulation ofBioscience reports · 2017Article
- The importance of the excitatory amino acid transporter 3 (EAAT3).Neurochemistry international · 2016Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Glutamate transporter type 3 (EAAT3) may play a role in cognition. Isoflurane enhances EAAT3 trafficking to the plasma membrane. Thus, we used isoflurane to determine how EAAT3 might regulate learning and memory and the trafficking of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, such as GluR1, to the plasma membrane, a fundamental biochemical process for learning and memory. Here, isoflurane increased EAAT3 but did not change GluR1 levels in the plasma membrane of wild-type mouse hippocampus. Isoflurane increased protein phosphatase activity in the wild-type and EAAT3(-/-) mouse hippocampus. Also, isoflurane reduced GluR1 in the plasma membrane and decreased phospho-GluR1 in EAAT3(-/-) mice. The phosphatase inhibitor okadaic acid attenuated these effects. Finally, isoflurane inhibited context-related fear conditioning in EAAT3(-/-) mice but not in wild-type mice. Thus, isoflurane may increase GluR1 trafficking to the plasma membrane via EAAT3 and inhibit GluR1 trafficking via protein phosphatase. Lack of EAAT3 effects leads to decreased GluR1 trafficking and impaired cognition after isoflurane exposure in EAAT3(-/-) mice.
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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.