Evidence map›Paper›PMID 27404844›Full record

ArticleExperimental neurology2016

Chemogenetic silencing of the midline and intralaminar thalamus blocks amygdala-kindled seizures.

Evan Wicker, Patrick A Forcelli

Abstract read
In one paragraph

Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Optogenetic stimulation of the dorsal striatum bidirectionally controls seizures.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Imaging-based chemogenetics for dissecting neural circuits in nonhuman primates.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Chemogenetics as a neuromodulatory approach to treating neuropsychiatric diseases and disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  13. DREADDs in Epilepsy Research: Network-Based Review.Frontiers in molecular neuroscience · 2022
    Review
  14. Review
  15. Distinct Fastigial Output Channels and Their Impact on Temporal Lobe Seizures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  16. Article
  17. Article
  18. The Subcortical-Allocortical- NeocorticalFrontiers in synaptic neuroscience · 2021
    Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Evan WickerDepartment of Pharmacology & Physiology, Georgetown University School of Medicine, United States.
Patrick A ForcelliDepartment of Pharmacology & Physiology, Georgetown University School of Medicine, United States. Electronic address: paf22@georgetown.edu.
Georgetown University · US

Funding

Institutional Career Development CoreKL2TR001432 · NCATS · GEORGETOWN UNIVERSITY · PI UMANS, JASON G · 2015 to 2024
$7.5M
NCATS NIH HHS KL2 TR001432
6 · The paper itself

Abstract

Temporal lobe epilepsy is the most common form of medically-intractable epilepsy. While seizures in TLE originate in structures such as hippocampus, amygdala, and temporal cortex, they propagate through a crucial relay: the midline/intralaminar thalamus. Prior studies have shown that pharmacological inhibition of midline thalamus attenuates limbic seizures. Here, we examined a recently developed technology, Designer Receptors Exclusively Activated by Designer Drugs (DREADDs), as a means of chemogenetic silencing to attenuate limbic seizures. Adult, male rats were electrically kindled from the amygdala, and injected with virus coding for inhibitory (hM4Di) DREADDs into the midline/intralaminar thalamus. When treated with the otherwise inert ligand Clozapine-N-Oxide (CNO) at doses of 2.5, 5, and 10mg/kg, electrographic and behavioral seizure manifestations were suppressed in comparison to vehicle. At higher doses, we found complete blockade of seizure activity in a subset of subjects. CNO displayed a sharp time-response profile, with significant seizure attenuation seen 20-30min post injection, in comparison to 10 and 40min post injection. Seizures in animals injected with a control vector (i.e., no DREADD) were unaffected by CNO administration. These data underscore the crucial role of the midline/intralaminar thalamus in the propagation of seizures, specifically in the amygdala kindling model, and provide validation of chemogenetic silencing of limbic seizures.

Indexed as

AmygdalaAnalysis of VarianceAnimalsAnticonvulsantsClozapineDisease Models, AnimalDose-Response Relationship, DrugElectric StimulationEvoked PotentialsIntralaminar Thalamic NucleiKindling, NeurologicMaleMaze LearningMidline Thalamic NucleiRatsRats, Sprague-DawleyAnticonvulsantsClozapineclozapine N-oxideAmygdalaChemogeneticCNODREADDKindlingRatSeizure

Identifiers

PMID27404844
PMCPMC4992629
OpenAlexW2469411888

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.