Evidence map›Paper›PMID 32086434›Full record

ReviewMolecular psychiatry2020

Prefrontal cortex circuits in depression and anxiety: contribution of discrete neuronal populations and target regions.

Brendan D Hare, Ronald S Duman

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06739304 (The Effectiveness of Mindfulness-based Relapse Prevention), which is not on this map. Cited by 194 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 3 pooled it
23.2field-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.

NCT06739304 nacompletednot on this mapstarted 2023, after this paper: background citation

The Effectiveness of Mindfulness-based Relapse Prevention: A Randomized Controlled Trial Study

TypeinterventionalSponsorSir Run Run Shaw HospitalRan2023 to 2023Enrolled1,200ConditionsSubstance Use DisorderArmsMindfulness-based Relapse Prevention
3 · Its place in the literature

Who cites it

194 citing papers in PubMed, 3 syntheses or guidelines pooled it, 357 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Modulation of early non-rapid eye movement slow wave activity by ketamine in treatment-resistant depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Trial
  5. Trial
  6. Article
  7. Article
  8. Review
  9. Review
  10. Converging on control: Rethinking treatment-resistant depression through network neuroscience.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  11. Article
  12. Article
  13. Sleep-anxiety symptom networks and subgroup characterization in nasopharyngeal carcinoma patients undergoing chemoradiotherapy: A latent profile and network analysis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
    Article
  14. Article
  15. Article
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  20. Network localization of brain functional effects of ketamine treatment for major depression.European psychiatry : the journal of the Association of European Psychiatrists · 2026
    Article

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

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.

Brendan D HareDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT, USA. Brendan.Hare@yale.edu.ORCID http://orcid.org/0000-0002-6502-3188
Ronald S DumanDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0001-8690-8439
Yale University · US

Funding

Role of mTOR and Synaptogenesis in the Actions of Rapid-Acting AntidepressantsR01MH093897 · NIMH · YALE UNIVERSITY · PI DILEONE, RALPH J · 2011 to 2021
$5.0M
Synaptic mechanisms underlying the rapid antidepressant actions of scopolamineR01MH105910 · NIMH · YALE UNIVERSITY · PI PICCIOTTO, MARINA R · 2014 to 2018
$2.2M
NIMH NIH HHS R01 MH093897NIMH NIH HHS R01 MH105910
6 · The paper itself

Abstract

Our understanding of depression and its treatment has advanced with the advent of ketamine as a rapid-acting antidepressant and the development and refinement of tools capable of selectively altering the activity of populations of neuronal subtypes. This work has resulted in a paradigm shift away from dysregulation of single neurotransmitter systems in depression towards circuit level abnormalities impacting function across multiple brain regions and neurotransmitter systems. Studies on the features of circuit level abnormalities demonstrate structural changes within the prefrontal cortex (PFC) and functional changes in its communication with distal brain structures. Treatments that impact the activity of brain regions, such as transcranial magnetic stimulation or rapid-acting antidepressants like ketamine, appear to reverse depression associated circuit abnormalities though the mechanisms underlying the reversal, as well as development of these abnormalities remains unclear. Recently developed optogenetic and chemogenetic tools that allow high-fidelity control of neuronal activity in preclinical models have begun to elucidate the contributions of the PFC and its circuitry to depression- and anxiety-like behavior. These tools offer unprecedented access to specific circuits and neuronal subpopulations that promise to offer a refined view of the circuit mechanisms surrounding depression and potential mechanistic targets for development and reversal of depression associated circuit abnormalities.

Indexed as

Neural PathwaysAntidepressive AgentsAnxietyDepressionKetaminePrefrontal CortexAntidepressive AgentsKetamine

Identifiers

PMID32086434
PMCPMC7442605
OpenAlexW3007694136

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.