Evidence map›Paper›PMID 27259067›Full record

ArticleEpilepsy research2016

Reduced expression of IA channels is associated with post-ischemic seizures.

Zhigang Lei, Hui Zhang, Yanling Liang, Zao C Xu

Abstract read
In one paragraph

Article in Epilepsy research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Role of UCHL1 in axonal injury and functional recovery after cerebral ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  6. Review
  7. Article
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.

Zhigang LeiDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA. Electronic address: zhlei@iupui.edu.
Hui ZhangDepartment of Pediatrics, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510150, People's Republic of China.
Yanling LiangDepartment of Neurology, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510150, People's Republic of China.
Zao C XuDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Indiana University School of MedicineThird Affiliated Hospital of Guangzhou Medical University · CN

Funding

The Mechanisms of Selective Cell Death After IschemiaR21NS071238 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI XU, ZAO C · 2010 to 2011
$419k
NINDS NIH HHS R21 NS071238
6 · The paper itself

Abstract

purposePost-stroke seizures are considered as a major cause of epilepsy in adults. The pathophysiologic mechanisms resulting in post-stroke seizures are not fully understood. The present study attempted to reveal a new mechanism underlying neuronal hyperexcitability responsible to the seizure development after ischemic stroke.

methodsTransient global ischemia was produced in adult Wistar rats using the 4-vessel occlusion (4-VO) method. The spontaneous behavioral seizures were defined by the Racine scale III-V. The neuronal death in the brain was determined by hematoxylin-eosin staining. The expression levels of A-type potassium channels were analyzed by immunohistochemical staining and western blotting.

resultsWe found that the incidence of spontaneous behavioral seizures increased according to the severity of ischemia with 0% after 15-min ischemia and ∼50% after 25-min ischemia. All behavioral seizures occurred with 48h after ischemia. Morphological analysis indicated that brain damage was not correlated with behavioral seizures. Immunohistochemical staining showed that the expression levels of the A-type potassium channel subunit Kv4.2 was significantly reduced in ischemic brains with behavioral seizures, but not in ischemic brains without seizures. In addition, rats failing to develop spontaneous behavioral seizures within 2days after ischemia were more sensitive to bicuculline-induced seizures at 2 months after ischemia than control rats. Meanwhile, Kv4.2 expression was decreased in brain at 2 months after ischemia.

conclusionOur results demonstrated the reduction of Kv4.2 expression might contribute to the development of post-ischemic seizures and long-term increased seizure susceptibility after ischemia. The mechanisms underlying post-stroke seizures and epilepsy is unknown so far. The down-regulation of IA channels may explained the abnormal neuronal hyperexcitability responsible for the seizure development after ischemic stroke.

Indexed as

AnimalsBicucullineBlotting, WesternBrainBrain IschemiaCell DeathDisease Models, AnimalDisease SusceptibilityGene ExpressionImmunohistochemistryKv Channel-Interacting ProteinsMaleNeuronsRats, WistarSeizuresSeverity of Illness IndexBicucullineKcnip2 protein, ratKv Channel-Interacting ProteinsShal Potassium ChannelsA-type potassium channelsEpilepsyEpileptogenesisExcitabilityKv4.2

Identifiers

PMID27259067
PMCPMC4915942
OpenAlexW2402218329

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.