Evidence map›Paper›PMID 23313318›Full record

ArticleNeurobiology of disease2013

Rapid surface accumulation of NMDA receptors increases glutamatergic excitation during status epilepticus.

David E Naylor, Hantao Liu, Jerome Niquet, Claude G Wasterlain

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

93 citing papers in PubMed, 1 synthesis or guideline pooled it, 206 citations in OpenAlex.

  1. Pooled it
  2. 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
    Review
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  4. Observational
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  13. Histamine HPharmacology research & perspectives · 2024
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33 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

David E NaylorDepartment of Neurology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, USA; Department of Neurology, Veterans Administration Greater Los Angeles Healthcare System, USA. dnaylor@ucla.edu
Hantao Liu
Jerome Niquet
Claude G Wasterlain
University of California, Los Angeles · USVA Greater Los Angeles Healthcare System · USWest Los Angeles College · US

Funding

Rational polytherapy in the treatment of cholinergic seizuresU01NS074926 · NINDS · BRENTWOOD BIOMEDICAL RESEARCH INSTITUTE · PI WASTERLAIN, CLAUDE G · 2011 to 2015
$3.3M
BRAIN DEVELOPMENT IN EXPERIMENTAL EPILEPSY: STATUSR01NS013515 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WASTERLAIN, CLAUDE G · 1986 to 2006
$2.2M
Treatment of Status Epilepticus: A Translational ProposalI01BX000273 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI WASTERLAIN, CLAUDE G · 2009 to 2017
–
BLRD VA I01 BX000273NINDS NIH HHS R01 NS013515NINDS NIH HHS U01 NS074926
6 · The paper itself

Abstract

After 1h of lithium-pilocarpine status epilepticus (SE), immunocytochemical labeling of NMDA receptor NR1 subunits reveals relocation of subunits from the interior to the cell surface of dentate gyrus granule cells and CA3 pyramidal cells. Simultaneously, an increase in NMDA-miniature excitatory postsynaptic currents (mEPSC) as well as an increase in NMDA receptor-mediated tonic currents is observed in hippocampal slices after SE. Mean-variance analysis of NMDA-mEPSCs estimates that the number of functional postsynaptic NMDA receptors per synapse increases 38% during SE, and antagonism by ifenprodil suggests that an increase in the surface representation of NR2B-containing NMDA receptors is responsible for the augmentation of both the phasic and tonic excitatory currents with SE. These results provide a potential mechanism for an enhancement of glutamatergic excitation that maintains SE and may contribute to excitotoxic injury during SE. Therapies that directly antagonize NMDA receptors may be a useful therapeutic strategy during refractory SE.

Indexed as

AnimalsDisease Models, AnimalExcitatory Postsynaptic PotentialsGlutamic AcidHippocampusImmunohistochemistryMalePatch-Clamp TechniquesProtein TransportRatsRats, WistarReceptors, N-Methyl-D-AspartateStatus EpilepticusSynapsesGlutamic AcidReceptors, N-Methyl-D-Aspartate

Identifiers

PMID23313318
PMCPMC5444936
OpenAlexW1978022925

What OpenQuestion holds

Textmetadata
LicenceTDM
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.