Evidence map›Paper›PMID 20091047›Full record

ReviewPflugers Archiv : European journal of physiology2010

Role of voltage-gated calcium channels in epilepsy.

Gerald W Zamponi, Philippe Lory, Edward Perez-Reyes

Open access · greenAbstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. The Role of Calcium Signaling in Sensorineural Hearing Loss.International journal of medical sciences · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. The Participation of CaCNS & neurological disorders drug targets · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

18 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Gerald W ZamponiDepartment of Physiology and Pharmacology, Hotchkiss Brain Institute, University of Calgary, Calgary, T2N 4N1, Canada.
Philippe Lory
Edward Perez-Reyes
Inserm · FRUniversity of Calgary · CAUniversity of Virginia · US

Funding

Mechanisms by which T-type calcium channels increase seizure susceptibilityR01NS067456 · NINDS · UNIVERSITY OF VIRGINIA · PI PEREZ-REYES, EDWARD · 2009 to 2010
$770k
NINDS NIH HHS NS067456NINDS NIH HHS R01 NS067456
6 · The paper itself

Abstract

It is well established that idiopathic generalized epilepsies (IGEs) show a polygenic origin and may arise from dysfunction of various types of voltage- and ligand-gated ion channels. There is an increasing body of literature implicating both high- and low-voltage-activated (HVA and LVA) calcium channels and their ancillary subunits in IGEs. Cav2.1 (P/Q-type) calcium channels control synaptic transmission at presynaptic nerve terminals, and mutations in the gene encoding the Cav2.1 alpha1 subunit (CACNA1A) have been linked to absence seizures in both humans and rodents. Similarly, mutations and loss of function mutations in ancillary HVA calcium channel subunits known to co-assemble with Cav2.1 result in IGE phenotypes in mice. It is important to note that in all these mouse models with mutations in HVA subunits, there is a compensatory increase in thalamic LVA currents which likely leads to the seizure phenotype. In fact, gain-of-function mutations have been identified in Cav3.2 (an LVA or T-type calcium channel encoded by the CACNA1H gene) in patients with congenital forms of IGEs, consistent with increased excitability of neurons as a result of enhanced T-type channel function. In this paper, we provide a broad overview of the roles of voltage-gated calcium channels, their mutations, and how they might contribute to the river that terminates in epilepsy.

Indexed as

AnimalsCalcium Channels, N-TypeCalcium Channels, T-TypeEpilepsyEpilepsy, AbsenceHumansMiceMice, Neurologic MutantsProtein SubunitsCACNA1H protein, humanCalcium Channels, N-TypeCalcium Channels, T-TypeProtein Subunits

Identifiers

PMID20091047
PMCPMC3312315
OpenAlexW1991289683

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.