Evidence map›Paper›PMID 21623007›Full record

ArticleJournal of neural engineering2011

High frequency stimulation abolishes thalamic network oscillations: an electrophysiological and computational analysis.

Kendall H Lee, Frederick L Hitti, Su-Youne Chang, Dongchul C Lee, David W Roberts, Cameron C McIntyre, James C Leiter

Open access · greenAbstract read
In one paragraph

Article in Journal of neural engineering, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 12% 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, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Towards network-guided neuromodulation for epilepsy.Brain : a journal of neurology · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Deep brain stimulation in Parkinson's disease.Translational neurodegeneration · 2013
    Article
  16. Review
  17. Modeling noninvasive neurostimulation in epilepsy as stochastic interference in brain networks.IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society · 2013
    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

7 authors at 3 institutions in 2 countries.

Kendall H LeeDepartment of Neurologic Surgery, Mayo Clinic, 200 First Street SW, Rochester, MN 55902, USA.
Frederick L Hitti
Su-Youne Chang
Dongchul C Lee
David W Roberts
Cameron C McIntyre
James C Leiter
Dartmouth College · USCleveland Clinic · USMayo Clinic · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007367 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI REINER, STEVEN L · 1985 to 2021
$25.1M
Mechanism of Action of Deep Brain StimulationK08NS052232 · NINDS · MAYO CLINIC ROCHESTER · PI LEE, KENDALL H. · 2008 to 2012
$857k
NIGMS NIH HHS T32 GM007367NINDS NIH HHS K08 NS052232
6 · The paper itself

Abstract

Deep brain stimulation (DBS) of the thalamus has been demonstrated to be effective for the treatment of epilepsy. To investigate the mechanism of action of thalamic DBS, we examined the effects of high frequency stimulation (HFS) on spindle oscillations in thalamic brain slices from ferrets. We recorded intracellular and extracellular electrophysiological activity in the nucleus reticularis thalami (nRt) and in thalamocortical relay (TC) neurons in the lateral geniculate nucleus, stimulated the slice using a concentric bipolar electrode, and recorded the level of glutamate within the slice. HFS (100 Hz) of TC neurons generated excitatory post-synaptic potentials, increased the number of action potentials in both TC and nRt neurons, reduced the input resistance, increased the extracellular glutamate concentration, and abolished spindle wave oscillations. HFS of the nRt also suppressed spindle oscillations. In both locations, HFS was associated with significant and persistent elevation in extracellular glutamate levels and suppressed spindle oscillations for many seconds after the cessation of stimulation. We simulated HFS within a computational model of the thalamic network, and HFS also disrupted spindle wave activity, but the suppression of spindle activity was short-lived. Simulated HFS disrupted spindle activity for prolonged periods of time only after glutamate release and glutamate-mediated activation of a hyperpolarization-activated current (I(h)) was incorporated into the model. Our results suggest that the mechanism of action of thalamic DBS as used in epilepsy may involve the prolonged release of glutamate, which in turn modulates specific ion channels such as I(h), decreases neuronal input resistance, and abolishes thalamic network oscillatory activity.

Indexed as

Action PotentialsAlgorithmsAnimalsBiosensing TechniquesCerebral CortexComputer SimulationCyclic Nucleotide-Gated Cation ChannelsDeep Brain StimulationElectrophysiological PhenomenaEpilepsyFemaleFerretsGlutamic AcidHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsInterneuronsMembrane PotentialsCyclic Nucleotide-Gated Cation ChannelsGlutamic AcidHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsPotassium Channels

Identifiers

PMID21623007
PMCPMC3155385
OpenAlexW2167016240

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.