Evidence map›Paper›PMID 29373121›Full record

ArticleBiological psychiatry2018

Thalamic Control of Cognition and Social Behavior Via Regulation of Gamma-Aminobutyric Acidergic Signaling and Excitation/Inhibition Balance in the Medial Prefrontal Cortex.

Brielle R Ferguson, Wen-Jun Gao

Abstract read
In one paragraph

Article in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing 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

113 citing papers in PubMed.

  1. Article
  2. Article
  3. Thalamocortical orchestration of human theory of mind.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Biomolecules · 2025
    Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Brielle R FergusonDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Wen-Jun GaoDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania. Electronic address: wg38@drexel.edu.

Funding

Development of NMDAR hypofunction and cognitive deficitsR01MH085666 · NIMH · DREXEL UNIVERSITY · PI GAO, WEN-JUN · 2009 to 2018
$3.8M
Targeting parvalbumin neurons in the PFC for cognitive deficitsR21MH111609 · NIMH · DREXEL UNIVERSITY · PI GAO, WEN-JUN · 2017 to 2018
$430k
Roles of NMDA receptors in schizophrenia pathological processR21MH079117 · NIMH · DREXEL UNIVERSITY · PI GAO, WEN-JUN · 2007 to 2008
$365k
Elucidation of the mediodorsal thalamic regulation of prefrontal functionF31MH111361 · NIMH · DREXEL UNIVERSITY · PI FERGUSON, BRIELLE · 2016 to 2017
$64k
NIMH NIH HHS F31 MH111361NIMH NIH HHS R01 MH085666NIMH NIH HHS R21 MH079117NIMH NIH HHS R21 MH111609
6 · The paper itself

Abstract

backgroundThe mediodorsal thalamus plays a critical role in cognition through its extensive innervation of the medial prefrontal cortex (mPFC), but how the two structures cooperate at the single-cell level to generate associated cognitive functions and other mPFC-dependent behaviors remains elusive. Maintaining the proper balance between excitation and inhibition (E/I balance) is of principal importance for organizing cortical activity. Furthermore, the PFC E/I balance has been implicated in successful execution of multiple PFC-dependent behaviors in both animal research and the context of human psychiatric disorders.

methodsHere, we used a pharmacogenetic strategy to decrease mediodorsal thalamic activity in adult male rats and evaluated the consequences for E/I balance in PFC pyramidal neurons as well as cognition, social interaction, and anxiety.

resultsWe found that dampening mediodorsal thalamic activity caused significant reductions in gamma-aminobutyric acidergic signaling and increased E/I balance in the mPFC and was concomitant with abnormalities in these behaviors. Furthermore, by selectively activating parvalbumin interneurons in the mPFC with a novel pharmacogenetic approach, we restored gamma-aminobutyric acidergic signaling and E/I balance as well as ameliorated all behavioral impairments.

conclusionsThese findings underscore the importance of thalamocortical activation of mPFC gamma-aminobutyric acidergic interneurons in a broad range of mPFC-dependent behaviors. Furthermore, they highlight this circuitry as a platform for therapeutic investigation in psychiatric diseases that involve impairments in PFC-dependent behaviors.

Indexed as

Social BehaviorAnimalsBehavior, AnimalCognitionExcitatory Postsynaptic PotentialsGABA AgentsGABAergic Neuronsgamma-Aminobutyric AcidInhibitory Postsynaptic PotentialsInterneuronsMaleMediodorsal Thalamic NucleusPatch-Clamp TechniquesPharmacogeneticsPrefrontal CortexRatsGABA Agentsgamma-Aminobutyric AcidCognitionGABAergic inhibitionPharmacogeneticsPrefrontal cortexPVIsSynaptic functionThalamus

Identifiers

PMID29373121
PMCPMC5862785

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

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 Socratic graph.