Evidence map›Paper›PMID 35508195›Full record

ReviewAnnual review of neuroscience2022

Synaptic Mechanisms Regulating Mood State Transitions in Depression.

Puja K Parekh, Shane B Johnson, Conor Liston

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
8.1field-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

55 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  3. Ferroptosis in depression: mechanisms, association, and therapeutic strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
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  6. FermentedFoods (Basel, Switzerland) · 2026
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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

3 authors at 2 institutions in 1 country.

Puja K ParekhDepartment of Psychiatry and Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York, USA; email: col2004@med.cornell.edu.
Shane B JohnsonDepartment of Psychiatry and Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York, USA; email: col2004@med.cornell.edu.
Conor ListonDepartment of Psychiatry and Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York, USA; email: col2004@med.cornell.edu.
MIND Research Institute · USWeill Cornell Medicine · US

Funding

Regulation of prefrontal cortical circuit function and reward-seeking behavior by stress-induced dendritic spine remodelingR01MH118451 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI Joshua Levitz, Conor M Liston · 2019 to 2026
$5.5M
Impact of BDNF on the Development of Social Behavior CircuitsR01MH123154 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI LEE, FRANCIS SANG YONG, LISTON, CONOR M · 2020 to 2024
$3.0M
Prefrontal Cortical Microcircuit Mechanisms of Working Memory Deficits in Chronic StressR01MH109685 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI LISTON, CONOR M · 2016 to 2020
$2.8M
Development of opioid and ketamine probes for in vivo photopharmacology (Diversity Supplement)RF1NS126073 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BANGHART, MATTHEW R., LISTON, CONOR M · 2022 to 2024
$2.0M
Corticostriatal and Corticoinsular Circuit Mechanisms Underlying Stress Effects on Effort-based Reward ProcessingK99MH127291 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI PAREKH, PUJA · 2021 to 2022
$242k
NIMH NIH HHS K99 MH127291NIMH NIH HHS R01 MH109685NIMH NIH HHS R01 MH118451NIMH NIH HHS R01 MH123154NINDS NIH HHS RF1 NS126073
6 · The paper itself

Abstract

Depression is an episodic form of mental illness characterized by mood state transitions with poorly understood neurobiological mechanisms. Antidepressants reverse the effects of stress and depression on synapse function, enhancing neurotransmission, increasing plasticity, and generating new synapses in stress-sensitive brain regions. These properties are shared to varying degrees by all known antidepressants, suggesting that synaptic remodeling could play a key role in depression pathophysiology and antidepressant function. Still, it is unclear whether and precisely how synaptogenesis contributes to mood state transitions. Here, we review evidence supporting an emerging model in which depression is defined by a distinct brain state distributed across multiple stress-sensitive circuits, with neurons assuming altered functional properties, synapse configurations, and, importantly, a reduced capacity for plasticity and adaptation. Antidepressants act initially by facilitating plasticity and enabling a functional reconfiguration of this brain state. Subsequently, synaptogenesis plays a specific role in sustaining these changes over time.

Indexed as

Antidepressive AgentsDepressionNeuronal PlasticityNeuronsSynapsesSynaptic TransmissionAntidepressive Agentsdendritic spinesdepressionketaminerapid-acting antidepressantsstresssynaptic plasticity

Identifiers

PMID35508195
PMCPMC11577286
OpenAlexW4229007163

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.