Evidence map›Paper›PMID 24804767›Full record

ArticlePloS one2014

Response of human thalamic neurons to high-frequency stimulation.

Merrill J Birdno, Wei Tang, Jonathan O Dostrovsky, William D Hutchison, Warren M Grill

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Neurophysiology and neural engineering: a review.Journal of neurophysiology · 2017
    Review
  9. Computational modeling to improve treatments for essential tremor.Drug discovery today. Disease models · 2016
    Article
  10. 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

5 authors.

Merrill J BirdnoDepartment of Biomedical Engineering, Duke University, Durham, North Carolina, United States of America.
Wei TangDepartment of Physiology, University of Toronto, Toronto, Ontario, Canada.
Jonathan O DostrovskyDepartment of Physiology, University of Toronto, Toronto, Ontario, Canada; Toronto Western Research Institute, Toronto, Ontario, Canada.
William D HutchisonDepartment of Physiology, University of Toronto, Toronto, Ontario, Canada; Toronto Western Research Institute, Toronto, Ontario, Canada.
Warren M GrillDepartment of Biomedical Engineering, Duke University, Durham, North Carolina, United States of America; Department of Electrical and Computer Engineering, Duke University, Durham, North Carolina, United States of America; Department of Neurobiology, Duke University, Durham, North Carolina, United States of America; Department of Surgery, Duke University, Durham, North Carolina, United States of America.

Funding

Temporal Patterns of Deep Brain StimulationR01NS040894 · NINDS · DUKE UNIVERSITY · PI GRILL, WARREN M. · 2000 to 2013
$3.4M
CIHR MOP-42505NINDS NIH HHS R01 NS040894NINDS NIH HHS US NIH R01 NS040894
6 · The paper itself

Abstract

Thalamic deep brain stimulation (DBS) is an effective treatment for tremor, but the mechanisms of action remain unclear. Previous studies of human thalamic neurons to noted transient rebound bursting activity followed by prolonged inhibition after cessation of high frequency extracellular stimulation, and the present study sought to identify the mechanisms underlying this response. Recordings from 13 thalamic neurons exhibiting low threshold spike (LTS) bursting to brief periods of extracellular stimulation were made during surgeries to implant DBS leads in 6 subjects with Parkinson's disease. The response immediately after cessation of stimulation included a short epoch of burst activity, followed by a prolonged period of silence before a return to LTS bursting. A computational model of a population of thalamocortical relay neurons and presynaptic axons terminating on the neurons was used to identify cellular mechanisms of the observed responses. The model included the actions of neuromodulators through inhibition of a non-pertussis toxin sensitive K(+) current (I(KL)), activation of a pertussis toxin sensitive K(+) current (I(KG)), and a shift in the activation curve of the hyperpolarization-activated cation current (I(h)). The model replicated well the measured responses, and the prolonged inhibition was associated most strongly with changes in I(KG) while modulation of I(KL) or I(h) had minimal effects on post-stimulus inhibition suggesting that neuromodulators released in response to high frequency stimulation are responsible for mediating the post-stimulation bursting and subsequent long duration silence of thalamic neurons. The modeling also indicated that the axons of the model neurons responded robustly to suprathreshold stimulation despite the inhibitory effects on the soma. The findings suggest that during DBS the axons of thalamocortical neurons are activated while the cell bodies are inhibited thus blocking the transmission of pathological signals through the network and replacing them with high frequency regular firing.

Indexed as

Action PotentialsComputational BiologyHumansModels, NeurologicalNeuronsThalamus

Identifiers

PMID24804767
PMCPMC4013084

What OpenQuestion holds

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Registered trials

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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.