Evidence map›Paper›PMID 21615728›Full record

ReviewBritish journal of pharmacology2012

HCN channelopathies: pathophysiology in genetic epilepsy and therapeutic implications.

Christopher A Reid, A Marie Phillips, Steven Petrou

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2012. 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
1.7field-weighted citation impact, top 17% 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, 59 citations in OpenAlex.

  1. Review
  2. Extracellular salt bridge networks around S4 implicated in HCN channel gating and heart disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Insights on the Role of Thalamocortical HCN Channels in Absence Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  9. Article
  10. Using a Multiplex Nucleic AcidFrontiers in molecular neuroscience · 2019
    Article
  11. Article
  12. IJournal of neurophysiology · 2018
    Article
  13. Article
  14. Review
  15. Article
  16. A Loss-of-FunctionFrontiers in molecular neuroscience · 2018
    Article
  17. Functional variants inEpilepsia open · 2017
    Article
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Christopher A ReidFlorey Neuroscience Institute and The Centre for Neuroscience, The University of Melbourne, Parkville, Victoria, Australia. careid@unimelb.edu.au
A Marie Phillips
Steven Petrou
University of Melbourne · AUFlorey Institute of Neuroscience and Mental Health · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperpolarization-activated cyclic nucleotide-gated channels (HCN) can act as pacemakers in the brain making them strong candidates for driving aberrant hypersynchronous network activity seen in epilepsy. Transcriptional changes in HCN channels occur in several animal models of epilepsy. However, only recently have genetic studies demonstrated sequence variation in HCN1 and HCN2 genes associated with human epilepsy. These include a triple proline deletion in HCN2 that increases channel function and occurs more often in patients with febrile seizure syndromes. Other HCNx gene variants have been described in idiopathic generalized epilepsy although the functional consequence of these remains unclear. In this review we explore potential cellular and network mechanisms involving HCN channels in the genetic epilepsies. We suggest how new genetic sequencing technology, medium-throughput functional assays and the ability to develop syndrome-specific animal models will provide a more comprehensive understanding of how I(h) contributes to pathogenic mechanisms underlying human genetic epilepsy. We also discuss what is known about the pharmacological manipulation of HCN channels in the context of epilepsy and how this may help future efforts in developing HCN-channel-based therapy.

Indexed as

Genetic Predisposition to DiseaseAnticonvulsantsCyclic Nucleotide-Gated Cation ChannelsEpilepsyGenetic VariationHumansHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsPotassium ChannelsAnticonvulsantsCyclic Nucleotide-Gated Cation ChannelsHCN1 protein, humanHCN2 protein, humanHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsPotassium Channels

Identifiers

PMID21615728
PMCPMC3252965
OpenAlexW1503574481

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.