Evidence map›Paper›PMID 24953239›Full record

ArticlePflugers Archiv : European journal of physiology2015

Thalamocortical neurons display suppressed burst-firing due to an enhanced Ih current in a genetic model of absence epilepsy.

Stuart M Cain, John R Tyson, Karen L Jones, Terrance P Snutch

Open access · hybridAbstract read
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 23% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Ontogeny of the Epileptic System in the Krushinsky-Molodkina Rat Strain with Genetically Determined Audiogenic Epilepsy.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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
  15. Article
  16. CaEpilepsia · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. Isolated P/Q Calcium Channel Deletion in Layer VI Corticothalamic Neurons Generates Absence Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    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 1 institution in 1 country.

Stuart M CainMichael Smith Laboratories and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, 219-2185 East Mall, Vancouver, BC, Canada, V6T 1Z4.
John R Tyson
Karen L Jones
Terrance P Snutch
University of British Columbia · CA

Funding

Canadian Institutes of Health Research 10677
6 · The paper itself

Abstract

Burst-firing in distinct subsets of thalamic relay (TR) neurons is thought to be a key requirement for the propagation of absence seizures. However, in the well-regarded Genetic Absence Epilepsy Rats from Strasbourg (GAERS) model as yet there has been no link described between burst-firing in TR neurons and spike-and-wave discharges (SWDs). GAERS ventrobasal (VB) neurons are a specific subset of TR neurons that do not normally display burst-firing during absence seizures in the GAERS model, and here, we assessed the underlying relationship of VB burst-firing with Ih and T-type calcium currents between GAERS and non-epileptic control (NEC) animals. In response to 200-ms hyperpolarizing current injections, adult epileptic but not pre-epileptic GAERS VB neurons displayed suppressed burst-firing compared to NEC. In response to longer duration 1,000-ms hyperpolarizing current injections, both pre-epileptic and epileptic GAERS VB neurons required significantly more hyperpolarizing current injection to burst-fire than those of NEC animals. The current density of the Hyperpolarization and Cyclic Nucleotide-activated (HCN) current (Ih) was found to be increased in GAERS VB neurons, and the blockade of Ih relieved the suppressed burst-firing in both pre-epileptic P15-P20 and adult animals. In support, levels of HCN-1 and HCN-3 isoform channel proteins were increased in GAERS VB thalamic tissue. T-type calcium channel whole-cell currents were found to be decreased in P7-P9 GAERS VB neurons, and also noted was a decrease in CaV3.1 mRNA and protein levels in adults. Z944, a potent T-type calcium channel blocker with anti-epileptic properties, completely abolished hyperpolarization-induced VB burst-firing in both NEC and GAERS VB neurons.

Indexed as

Action PotentialsAnimalsCalcium Channel BlockersCalcium Channels, T-TypeCerebral CortexEpilepsy, AbsenceFemaleHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsInterneuronsMaleRatsRNA, MessengerThalamusCalcium Channel BlockersCalcium Channels, T-TypeHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsRNA, Messenger

Identifiers

PMID24953239
PMCPMC4435665
OpenAlexW2012639627

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.