Evidence map›Paper›PMID 30039334›Full record

ArticleMolecular neurobiology2019

Perampanel but Not Amantadine Prevents Behavioral Alterations and Epileptogenesis in Pilocarpine Rat Model of Status Epilepticus.

Hanan Mohammad, Sathiya Sekar, Zelan Wei, Farzad Moien-Afshari, Changiz Taghibiglou

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. 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
1.9field-weighted citation impact, top 15% 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, 36 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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  9. Deregulation of Astroglial TASK-1 KInternational journal of molecular sciences · 2023
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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

5 authors at 2 institutions in 1 country.

Hanan MohammadDepartment of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, S7N 5E5, Canada.
Sathiya SekarDepartment of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, S7N 5E5, Canada.
Zelan WeiDepartment of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, S7N 5E5, Canada.
Farzad Moien-AfshariDepartment of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, S7N 5E5, Canada. Farzad.MoienAfshari@vch.ca.
Changiz TaghibiglouDepartment of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, S7N 5E5, Canada. changiz.taghibiglou@usask.ca.ORCID http://orcid.org/0000-0002-4527-7404
University of Saskatchewan · CAUniversity of British Columbia · CA

Funding

Saskatchewan Health Research Foundation SHRF #3543
6 · The paper itself

Abstract

Pilocarpine-induced status epilepticus (SE), which results in the development of spontaneous recurrent seizures (SRSs) activates glutamatergic receptors that contribute to seizure sustenance and neuronal cell death. In the current study, we evaluate whether the exposure to perampanel, an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor blocker, or amantadine, a N-methyl-D-aspartic acid (NMDA) receptor blocker would reduce the SE-induced long-term consequences. SE was induced in adult male Sprague Dawley rats with pilocarpine. Perampanel or amantadine was injected 10 or 60 min after SE onset. The efficacy of either, in overcoming pilocarpine-induced SE was assessed using electroencephalogram (EEG) recordings. In addition, alterations in cognitive function, development of spontaneous recurrent seizures (SRSs), and hippocampal damage that are generally encountered after SE were also assessed at 72 h and 5 weeks after the induction of SE. Our results indicate that both early and late treatment with perampanel but not amantadine significantly reduced seizure activity. Furthermore, perampanel but not amantadine, reversed the memory deficits in Y-maze and novel object recognition (NOR) tests and retarded the appearance of SRSs. Moreover, perampanel treatment led to reduced SE-induced caspase-3 activation in the hippocampal lysates. Taken together, the data obtained from the study reveals that blocking AMPA receptors by perampanel can modify SE-induced long-term consequences. Our results may provide a proof of principle for the potential therapeutic application of perampanel in clinical use for status epilepticus in future.

Indexed as

Behavior, AnimalAmantadineAnimalsAstrocytesCaspase 3Cell SurvivalCognition DisordersDisease Models, AnimalEnzyme ActivationMaleNeuronsNitrilesPilocarpineProtein SubunitsPyridonesRats, Sprague-DawleyAmantadineCaspase 3glutamate receptor ionotropic, AMPA 2NitrilesperampanelPilocarpineProtein SubunitsPyridonesReceptors, AMPAAMPA receptorNMDA receptorSpatial memoryStatus epilepticus

Identifiers

PMID30039334
OpenAlexW2884095362

What OpenQuestion holds

Textmetadata
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.