Evidence map›Paper›PMID 26896834›Full record

ArticleExperimental neurology2016

Repeated low-dose kainate administration in C57BL/6J mice produces temporal lobe epilepsy pathology but infrequent spontaneous seizures.

Anthony D Umpierre, Isaiah V Bennett, Lismore D Nebeker, Thomas G Newell, Bruce B Tian, Kyle E Thomson, H Steve White, John A White, Karen S Wilcox

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Neonatal microglia replacement in mice modulates seizure severity in adulthood.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  8. Microglial P2YNeuron · 2024
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  15. CBP Is Required for Establishing Adaptive Gene Programs in the Adult Mouse Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  16. Article
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  20. 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

9 authors at 3 institutions in 1 country.

Anthony D UmpierreInterdepartmental Program in Neuroscience, University of Utah, 401 MREB, 20N. 1900E, Salt Lake City, UT 84132, United States. Electronic address: Anthony.Umpierre@utah.edu.
Isaiah V BennettDept. of Pharmacology & Toxicology, University of Utah, College of Pharmacy, 30N. 1900E, Salt Lake City, UT 84112, United States. Electronic address: isaiahvbennett98@gmail.com.
Lismore D NebekerDept. of Pharmacology & Toxicology, University of Utah, College of Pharmacy, 30N. 1900E, Salt Lake City, UT 84112, United States. Electronic address: U0879974@utah.edu.
Thomas G NewellAnticonvulsant Drug Development Program, University of Utah, 417 Wakara Way, Suite 3211, Salt Lake City, UT 84108, United States; Dept. of Bioengineering, University of Utah, 36S. Wasatch Drive, Rm. 3100, Salt Lake City, UT 84112, United States. Electronic address: Thomas.Newell@utah.edu.
Bruce B TianDept. of Pharmacology & Toxicology, University of Utah, College of Pharmacy, 30N. 1900E, Salt Lake City, UT 84112, United States. Electronic address: U0667419@utah.edu.
Kyle E ThomsonAnticonvulsant Drug Development Program, University of Utah, 417 Wakara Way, Suite 3211, Salt Lake City, UT 84108, United States; Dept. of Bioengineering, University of Utah, 36S. Wasatch Drive, Rm. 3100, Salt Lake City, UT 84112, United States. Electronic address: K.Thomson@utah.edu.
H Steve WhiteDept. of Pharmacology & Toxicology, University of Utah, College of Pharmacy, 30N. 1900E, Salt Lake City, UT 84112, United States; Anticonvulsant Drug Development Program, University of Utah, 417 Wakara Way, Suite 3211, Salt Lake City, UT 84108, United States; Department of Pharmacy, University of Washington, Box 357630, H375 Health Science Building, Seattle, WA 98195, United States. Electronic address: hswhite@uw.edu.
John A WhiteDept. of Biomedical Engineering, Boston University, 44 Cummington Mall, Rm. 403, Boston, MA 02215, United States. Electronic address: jwhite@bu.edu.
Karen S WilcoxInterdepartmental Program in Neuroscience, University of Utah, 401 MREB, 20N. 1900E, Salt Lake City, UT 84132, United States; Dept. of Pharmacology & Toxicology, University of Utah, College of Pharmacy, 30N. 1900E, Salt Lake City, UT 84112, United States; Anticonvulsant Drug Development Program, University of Utah, 417 Wakara Way, Suite 3211, Salt Lake City, UT 84108, United States. Electronic address: Karen.Wilcox@hsc.utah.edu.
University of Utah · USBoston University · USUniversity of Washington · US

Funding

Calcium Signaling in a Model of Temporal Lobe EpilepsyR01NS078331 · NINDS · UNIVERSITY OF UTAH · PI WHITE, JOHN A., WILCOX, KAREN S · 2012 to 2016
$2.0M
Predoctoral Interdepartmental Training Program in NeuroscienceT32NS076067 · NINDS · UNIVERSITY OF UTAH · PI KEEFE, KRISTEN A · 2011 to 2015
$1.1M
NINDS NIH HHS HHSN271201100029CNINDS NIH HHS R01 NS078331NINDS NIH HHS T32 NS076067PHS HHS HHSN 271201100029C
6 · The paper itself

Abstract

More efficient or translationally relevant approaches are needed to model acquired temporal lobe epilepsy (TLE) in genetically tractable mice. The high costs associated with breeding and maintaining transgenic, knock-in, or knock-out lines place a high value on the efficiency of induction and animal survivability. Herein, we describe our approaches to model acquired epilepsy in C57BL/6J mice using repeated, low-dose kainate (KA) administration paradigms. Four paradigms (i.p.) were tested for their ability to induce status epilepticus (SE), temporal lobe pathology, and the development of epilepsy. All four paradigms reliably induce behavioral and/or electrographic SE without mortality over a 7d period. Two of the four paradigms investigated produce features indicative of TLE pathology, including hippocampal cell death, widespread astrogliosis, and astrocyte expression of mGluR5, a feature commonly reported in TLE models. Three of the investigated paradigms were able to produce aberrant electrographic features, such as interictal spiking in cortex. However, only one paradigm, previously published by others, produces spontaneous recurrent seizures over an eight week period. Presentation of spontaneous seizures is rare (N=2/14), with epilepsy preferentially developing in animals having a high number of seizures during SE. Overall, repeated, low-dose KA administration improves the efficiency and pathological relevance of a systemic KA insult, but does not produce a robust epilepsy phenotype under the experimental paradigms described herein.

Indexed as

AnimalsAstrocytesCell DeathDisease Models, AnimalElectroencephalographyEpilepsy, Temporal LobeExcitatory Amino Acid AgonistsGlial Fibrillary Acidic ProteinGliosisHippocampusKainic AcidMaleMiceMice, Inbred C57BLReceptor, Metabotropic Glutamate 5SeizuresExcitatory Amino Acid AgonistsGlial Fibrillary Acidic ProteinGrm5 protein, mouseKainic AcidReceptor, Metabotropic Glutamate 5AstrogliosisC57 (C57BL/6J)Cell deathKainatemGluR5NeurodegenerationSeizureTemporal lobe epilepsyValproic acid

Identifiers

PMID26896834
PMCPMC5382800
OpenAlexW2286184715

What OpenQuestion holds

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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.