Evidence map›Paper›PMID 23143518›Full record

ArticleNature neuroscience2013

Closed-loop optogenetic control of thalamus as a tool for interrupting seizures after cortical injury.

Jeanne T Paz, Thomas J Davidson, Eric S Frechette, Bruno Delord, Isabel Parada, Kathy Peng, Karl Deisseroth, John R Huguenard

Abstract read
In one paragraph

Article in Nature neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 294 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
294citing papers in PubMed, 1 pooled it
17.0field-weighted citation impact, top 1% 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

294 citing papers in PubMed, 1 synthesis or guideline pooled it, 569 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Hemodynamic and Electrophysiological Progression of the Rose Bengal Photothrombotic Stroke Model in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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  17. Article
  18. Biomarkers for Epilepsy Deep Brain Stimulation.Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society · 2025
    Review
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Jeanne T PazDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA.
Thomas J Davidson
Eric S Frechette
Bruno Delord
Isabel Parada
Kathy Peng
Karl Deisseroth
John R Huguenard
Stanford University · USInstitut Systèmes Intelligents et de Robotique · FR

Funding

Inhibitory Controls of Thalamic NeuronsR01NS034774 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1996 to 2021
$5.5M
CELLULAR MECHANISMS IN FOCAL EPILEPTOGENESISR01NS006477 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1985 to 2013
$5.0M
Role of Thalamus in Post-stroke epileptogenesisK99NS078118 · NINDS · STANFORD UNIVERSITY · PI PAZ, JEANNE T · 2012 to 2013
$179k
Howard Hughes Medical InstituteNINDS NIH HHS 5R01NS006477NINDS NIH HHS 5R01NS034774NINDS NIH HHS K99 NS078118NINDS NIH HHS K99NS078118-01NINDS NIH HHS R01 NS006477NINDS NIH HHS R01 NS034774
6 · The paper itself

Abstract

Cerebrocortical injuries such as stroke are a major source of disability. Maladaptive consequences can result from post-injury local reorganization of cortical circuits. For example, epilepsy is a common sequela of cortical stroke, but the mechanisms responsible for seizures following cortical injuries remain unknown. In addition to local reorganization, long-range, extra-cortical connections might be critical for seizure maintenance. In rats, we found that the thalamus, a structure that is remote from, but connected to, the injured cortex, was required to maintain cortical seizures. Thalamocortical neurons connected to the injured epileptic cortex underwent changes in HCN channel expression and became hyperexcitable. Targeting these neurons with a closed-loop optogenetic strategy revealed that reducing their activity in real-time was sufficient to immediately interrupt electrographic and behavioral seizures. This approach is of therapeutic interest for intractable epilepsy, as it spares cortical function between seizures, in contrast with existing treatments, such as surgical lesioning or drugs.

Indexed as

OptogeneticsAction PotentialsAge FactorsAnimalsAnimals, NewbornBiophysical PhenomenaBiophysicsBrain InjuriesCalcium-Calmodulin-Dependent Protein Kinase Type 2Cerebral CortexCyclic Nucleotide-Gated Cation ChannelsDisease Models, AnimalElectric CapacitanceElectric StimulationElectroencephalographyHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsbiocytinCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, ratCyclic Nucleotide-Gated Cation ChannelsHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsLuminescent ProteinsLysine

Identifiers

PMID23143518
PMCPMC3700812
OpenAlexW2156108573

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.