Evidence map›Paper›PMID 22405820›Full record

ArticleBiochemical and biophysical research communications2012

Hyperpolarization-activated cation current Ih of dentate gyrus granule cells is upregulated in human and rat temporal lobe epilepsy.

Rainer Surges, Maria Kukley, Amy Brewster, Christiane Rüschenschmidt, Johannes Schramm, Tallie Z Baram, Heinz Beck, Dirk Dietrich

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 29% 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, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  15. Article
  16. Review
  17. Using a Multiplex Nucleic AcidFrontiers in molecular neuroscience · 2019
    Article
  18. Article
  19. Functional variants inEpilepsia open · 2017
    Article
  20. 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

8 authors at 2 institutions in 2 countries.

Rainer SurgesDepartment of Epileptology, University of Bonn Medical Center, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. rainer.surges@googlemail.com
Maria Kukley
Amy Brewster
Christiane Rüschenschmidt
Johannes Schramm
Tallie Z Baram
Heinz Beck
Dirk Dietrich
University of Bonn · DEUniversity of California, Irvine · US

Funding

FEBRILE SEIZURE MODEL--NEURONAL INJURY AND MECHANISMSR01NS035439 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARAM, TALLIE Z. · 1997 to 2018
$3.2M
Febrile Seizure Model - Neuronal Injury and MechanismsR37NS035439 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARAM, TALLIE Z. · 2006 to 2012
$2.6M
NINDS NIH HHS NS35439NINDS NIH HHS R01 NS035439NINDS NIH HHS R37 NS035439
6 · The paper itself

Abstract

The hyperpolarization-activated cation current I(h) is an important regulator of neuronal excitability and may contribute to the properties of the dentate gyrus granule (DGG) cells, which constitute the input site of the canonical hippocampal circuit. Here, we investigated changes in I(h) in DGG cells in human temporal lobe epilepsy (TLE) and the rat pilocarpine model of TLE using the patch-clamp technique. Messenger-RNA (mRNA) expression of I(h)-conducting HCN1, 2 and 4 isoforms was determined using semi-quantitative in-situ hybridization. I(h) density was ∼1.8-fold greater in DGG cells of TLE patients with Ammon's horn sclerosis (AHS) as compared to patients without AHS. The magnitude of somatodendritic I(h) was enhanced also in DGG cells in epileptic rats, most robustly during the latent phase after status epilepticus and prior to the occurrence of spontaneous epileptic seizures. During the chronic phase, I(h) was increased ∼1.7-fold. This increase of I(h) was paralleled by an increase in HCN1 and HCN4 mRNA expression, whereas HCN2 expression was unchanged. Our data demonstrate an epilepsy-associated upregulation of I(h) likely due to increased HCN1 and HCN4 expression, which indicate plasticity of I(h) during epileptogenesis and which may contribute to a compensatory decrease in neuronal excitability of DGG cells.

Indexed as

AnimalsCells, CulturedCyclic Nucleotide-Gated Cation ChannelsDentate GyrusDisease Models, AnimalEpilepsy, Temporal LobeHumansHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsNeuronsPatch-Clamp TechniquesPilocarpinePotassium ChannelsRatsUp-RegulationCyclic Nucleotide-Gated Cation ChannelsHCN1 protein, humanHcn1 protein, ratHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsPilocarpinePotassium Channels

Identifiers

PMID22405820
PMCPMC3383809
OpenAlexW2025671182

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.