ArticleNeurobiology of disease2017
Enhanced AMPA receptor-mediated neurotransmission on CA1 pyramidal neurons during status epilepticus.
Article in Neurobiology of disease, 2017. 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, 63 citations in OpenAlex.
- Neuroplastin Suppresses Seizures by Downregulating Endophilin A1 to Promote Internalization of GluA1-AMPA Receptors: Therapeutic Implications of Arbutin.Neuroscience bulletin · 2026Article
- Overactive EAAT1 ClActa neuropathologica communications · 2026Article
- Hydroxycarboxylic Acid Receptor 2 Mediates β-hydroxybutyrate's Antiseizure Effect in Mice.Annals of neurology · 2026Article
- Article
- Status epilepticus: Updates on mechanisms and treatments.Epilepsia open · 2025Review
- The VGCC auxiliary subunit α2δ1 is an extracellular GluA1 interactor and regulates LTP, spatial memory, and seizure susceptibility.bioRxiv : the preprint server for biology · 2024Article
- Targeted sonogenetic modulation of GABAergic interneurons in the hippocampal CA1 region in status epilepticus.Theranostics · 2024Article
- Neuronal plasticity contributes to postictal death.Progress in neurobiology · 2023Article
- Alterations in Rat Hippocampal Glutamatergic System Properties after Prolonged Febrile Seizures.International journal of molecular sciences · 2023Article
- Febrile Seizures Cause a Rapid Depletion of Calcium-Permeable AMPA Receptors at the Synapses of Principal Neurons in the Entorhinal Cortex and Hippocampus of the Rat.International journal of molecular sciences · 2023Article
- In the fast lane: Receptor trafficking during status epilepticus.Epilepsia open · 2023Review
- Treatment of status epilepticus: Physiology, pharmacology, and future directions.Epilepsia open · 2023Article
- Increased glutamatergic synaptic transmission during development in layer II/III mouse motor cortex pyramidal neurons.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Why ketamine.Epilepsy & behavior : E&B · 2023Review
- The Roles of Glutamate Receptors and Their Antagonists in Status Epilepticus, Refractory Status Epilepticus, and Super-Refractory Status Epilepticus.Biomedicines · 2023Review
- Critical involvement of lysyl oxidase in seizure-induced neuronal damage through ERK-Alox5-dependent ferroptosis and its therapeutic implications.Acta pharmaceutica Sinica. B · 2022Article
- Neuronal circuits sustaining neocortical-injury-induced status epilepticus.Neurobiology of disease · 2022Article
- Impairments of Long-Term Synaptic Plasticity in the Hippocampus of Young Rats during the Latent Phase of the Lithium-Pilocarpine Model of Temporal Lobe Epilepsy.International journal of molecular sciences · 2021Article
- Insertion of Calcium-Permeable AMPA Receptors during Epileptiform Activity In Vitro Modulates Excitability of Principal Neurons in the Rat Entorhinal Cortex.International journal of molecular sciences · 2021Article
- Short-Term Epileptiform Activity Potentiates Excitatory Synapses but Does Not Affect Intrinsic Membrane Properties of Pyramidal Neurons in the Rat Hippocampus In Vitro.Biomedicines · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Status epilepticus (SE) is a common neurological emergency that results from the failure of the mechanisms responsible for seizure termination or the initiation of mechanisms that lead to abnormally prolonged seizures. Although the failure of inhibitory mechanisms during SE is well understood, the seizure-initiating mechanisms are poorly understood. We tested whether hippocampal α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated transmission was enhanced during SE and assessed the underlying molecular mechanism. In animals in self-sustaining limbic SE the amplitudes of the miniature, spontaneous, and AMPA-evoked excitatory currents recorded from the CA1 pyramidal neurons were larger than those recorded in the controls. The evoked EPSCs rectified inwardly. In these animals, the surface expression of GluA1 subunit-containing AMPARs was increased in the CA1 pyramidal neurons. The phosphorylation of the GluA1 subunit on S831 and S845 residues was reduced in animals in SE. In contrast, the GluA1 subunit surface expression and AMPAR-mediated neurotransmission of dentate granule cells (DGCs) was not altered. Treating animals in SE with the NMDAR antagonist MK-801 or with diazaepam blocked the increased surface expression of the GluA1 subunits. NMDAR blockade also prevented the dephosphorylation of the S845 residue but not that of S831. Targeting NMDARs and AMPARs may provide novel strategies to treat benzodiazepine-refractory SE.
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