Evidence map›Paper›PMID 30507615›Full record

ArticleThe Journal of clinical investigation2019

Chemogenetic silencing of hippocampal neurons suppresses epileptic neural circuits.

Qi-Gang Zhou, Ashley D Nemes, Daehoon Lee, Eun Jeoung Ro, Jing Zhang, Amy S Nowacki, Susan M Dymecki, Imad M Najm, Hoonkyo Suh

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Hippocampal Chandelier Cells Modulate Seizure Susceptibility and Severity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Chemogenetics with PSAMGene therapy · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Increasing adult-born neurons protects mice from epilepsy.bioRxiv : the preprint server for biology · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. TheThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    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

9 authors at 4 institutions in 2 countries.

Qi-Gang ZhouDepartment of Neurosciences, Cleveland Clinic, Cleveland, Ohio, USA.
Ashley D NemesEpilepsy Center, Neurological Institute, and.
Daehoon LeeDepartment of Neurosciences, Cleveland Clinic, Cleveland, Ohio, USA.
Eun Jeoung RoDepartment of Neurosciences, Cleveland Clinic, Cleveland, Ohio, USA.
Jing ZhangDepartment of Clinical Pharmacology, Pharmacy College, Nanjing Medical University, Nanjing, China.
Amy S NowackiDepartment of Quantitative Health Sciences, Cleveland Clinic, Cleveland, Ohio, USA.
Susan M DymeckiDepartment of Genetics, Harvard Medical School, Boston, Massachusetts, USA.
Imad M NajmEpilepsy Center, Neurological Institute, and.
Hoonkyo SuhDepartment of Neurosciences, Cleveland Clinic, Cleveland, Ohio, USA.
Cleveland Clinic · USThe Neurological Institute · USHarvard University · USNanjing Medical University · CN

Funding

Alcohol-induced neurogenesisR01AA022377 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI SUH, HOONKYO · 2014 to 2018
$1.8M
NIAAA NIH HHS R01 AA022377
6 · The paper itself

Abstract

We investigated how pathological changes in newborn hippocampal dentate granule cells (DGCs) lead to epilepsy. Using a rabies virus-mediated retrograde tracing system and a designer receptors exclusively activated by designer drugs (DREADD) chemogenetic method, we demonstrated that newborn hippocampal DGCs are required for the formation of epileptic neural circuits and the induction of spontaneous recurrent seizures (SRS). A rabies virus-mediated mapping study revealed that aberrant circuit integration of hippocampal newborn DGCs formed excessive de novo excitatory connections as well as recurrent excitatory loops, allowing the hippocampus to produce, amplify, and propagate excessive recurrent excitatory signals. In epileptic mice, DREADD-mediated-specific suppression of hippocampal newborn DGCs dramatically reduced epileptic spikes and SRS in an inducible and reversible manner. Conversely, specific activation of hippocampal newborn DGCs increased both epileptic spikes and SRS. Our study reveals an essential role for hippocampal newborn DGCs in the formation and function of epileptic neural circuits, providing critical insights into DGCs as a potential therapeutic target for treating epilepsy.

Indexed as

AnimalsAnimals, NewbornDentate GyrusDesigner DrugsEpilepsyMaleMiceMice, TransgenicNerve NetDesigner DrugsEpilepsyNeuronal stem cellsNeuroscienceStem cells

Identifiers

PMID30507615
PMCPMC6307945
OpenAlexW2903164850

What OpenQuestion holds

Textmetadata
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.