Evidence map›Paper›PMID 20226181›Full record

ArticleExperimental neurology2010

Activation of ERK by spontaneous seizures in neural progenitors of the dentate gyrus in a mouse model of epilepsy.

Yi Li, Zechun Peng, Bo Xiao, Carolyn R Houser

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Ras-MAPK somatic variants in mesial temporal lobe epilepsy.Current opinion in genetics & development · 2026
    Review
  2. Article
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  11. miR-217-casein kinase-2 cross talk regulates ERK activation in ganglioglioma.Journal of molecular medicine (Berlin, Germany) · 2017
    Article
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  15. Review
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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 2 institutions in 2 countries.

Yi LiDepartment of Neurobiology, CHS 73-235, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, CA 90095-1763, USA.
Zechun Peng
Bo Xiao
Carolyn R Houser
University of California, Los Angeles · USXiangya Hospital Central South University · CN

Funding

GABA Neurons and EpilepsyR01NS046524 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HOUSER, CAROLYN R · 2003 to 2007
$1.6M
Neuronal Loss and Plasticity in EpilepsyI01BX000404 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI HOUSER, CAROLYN R · 2011 to 2013
–
BLRD VA I01 BX000404NINDS NIH HHS NS046524NINDS NIH HHS R01 NS046524
6 · The paper itself

Abstract

Cellular changes that are associated with spontaneous seizures in temporal lobe epilepsy are not well understood but could influence ongoing epilepsy-related processes. In order to identify cell signaling events that could occur at the time of spontaneous seizures, the localization of phosphorylated extracellular signal-regulated kinase (pERK) was studied in a pilocarpine mouse model of epilepsy at very short intervals (1.5-2.5 min) after detection of a spontaneous seizure. Within the hippocampal formation, immunolabeling of pERK was evident in a subpopulation of cells in the subgranular zone (SGZ) of the dentate gyrus at these short intervals. Many of these cells had a long vertical process and resembled radial glia, while others had short processes and were oriented horizontally. Labeling with a series of developmental markers demonstrated that virtually all pERK-labeled cells were neural progenitor cells (NPCs). A high percentage ( approximately 80%) of the pERK-labeled cells was labeled with either glial fibrillary acidic protein or brain lipid binding protein, indicating that these cells were radial glia-like NPCs. A smaller percentage of labeled cells expressed NeuroD, suggesting that they were later-developing NPCs that were assuming a neuronal identity. Early expression of pERK was not detected in immature neurons. Double labeling with proliferation markers demonstrated that approximately 30% of pERK-labeled NPCs expressed Mcm2, indicating that they were actively proliferating. Furthermore, virtually all radial glia-like NPCs that were in the proliferative cycle expressed pERK. These findings suggest that spontaneous seizures and associated ERK activation could contribute to the proliferation of radial glia-like NPCs in this epilepsy model.

Indexed as

AnimalsCell CountDentate GyrusDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesGlial Fibrillary Acidic ProteinImmunohistochemistryMaleMiceMice, Inbred C57BLMicroscopy, ConfocalNeurogenesisNeurogliaNeuronsPhosphorylationPilocarpineExtracellular Signal-Regulated MAP KinasesGlial Fibrillary Acidic ProteinPilocarpine

Identifiers

PMID20226181
PMCPMC2893891
OpenAlexW2027673318

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.