Evidence map›Paper›PMID 36861477›Full record

ReviewEpilepsia open2023

In the fast lane: Receptor trafficking during status epilepticus.

David E Naylor

Open access · goldAbstract readReview
In one paragraph

Review in Epilepsia open, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Perampanel as a candidate for polytherapy in Stage 1 Plus status epilepticus: biological rationale and translational limits.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  7. Treatment considerations for the management of neonatal onset seizures.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2025
    Article
  8. Article
  9. Review
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  12. Article
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  14. Status epilepticus in the neonate.BMJ paediatrics open · 2025
    Review
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  17. Selective modulation of epileptic tissue by an adenosine ABritish journal of pharmacology · 2024
    Article
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

David E NaylorVA Greater Los Angeles Healthcare System, Department of Neurology, David Geffen School of Medicine at UCLA, and The Lundquist Institute at Harbor-UCLA Medical Center, Los Angeles, California, USA.ORCID 0000-0002-6054-1795
VA Greater Los Angeles Healthcare System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Status epilepticus (SE) remains a significant cause of morbidity and mortality and often is refractory to standard first-line treatments. A rapid loss of synaptic inhibition and development of pharmacoresistance to benzodiazepines (BZDs) occurs early during SE, while NMDA and AMPA receptor antagonists remain effective treatments after BZDs have failed. Multimodal and subunit-selective receptor trafficking within minutes to an hour of SE involves GABA-A, NMDA, and AMPA receptors and contributes to shifts in the number and subunit composition of surface receptors with differential impacts on the physiology, pharmacology, and strength of GABAergic and glutamatergic currents at synaptic and extrasynaptic sites. During the first hour of SE, synaptic GABA-A receptors containing γ2 subunits move to the cell interior while extrasynaptic GABA-A receptors with δ subunits are preserved. Conversely, NMDA receptors containing N2B subunits are increased at synaptic and extrasynaptic sites, and homomeric GluA1 ("GluA2-lacking") calcium permeant AMPA receptor surface expression also is increased. Molecular mechanisms, largely driven by NMDA receptor or calcium permeant AMPA receptor activation early during circuit hyperactivity, regulate subunit-specific interactions with proteins involved with synaptic scaffolding, adaptin-AP2/clathrin-dependent endocytosis, endoplasmic reticulum (ER) retention, and endosomal recycling. Reviewed here is how SE-induced shifts in receptor subunit composition and surface representation increase the excitatory to inhibitory imbalance that sustains seizures and fuels excitotoxicity contributing to chronic sequela such as "spontaneous recurrent seizures" (SRS). A role for early multimodal therapy is suggested both for treatment of SE and for prevention of long-term comorbidities.

Indexed as

Receptors, GABA-AStatus EpilepticusBenzodiazepinesHumansN-MethylaspartateReceptors, AMPAReceptors, N-Methyl-D-AspartateSeizuresBenzodiazepinesN-MethylaspartateReceptors, AMPAReceptors, GABA-AReceptors, N-Methyl-D-AspartateAMPAepilepsyGABANMDAphosphorylationseizure

Identifiers

PMID36861477
PMCPMC10173858
OpenAlexW4322758054

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.