Evidence map›Paper›PMID 23036622›Full record

ReviewNeuroscience2013

Remodeling of axo-spinous synapses in the pathophysiology and treatment of depression.

P Licznerski, R S Duman

Abstract readReview
In one paragraph

Review in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
–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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  8. Mechanisms of SSRI Therapy and Discontinuation.Current topics in behavioral neurosciences · 2024
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19 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.

P LicznerskiDivision of Molecular Psychiatry, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, Yale University School of Medicine, New Haven, CT 06508, United States.
R S Duman

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
Antidepressants: Signal Transduction and Gene ExpressionR37MH045481 · NIMH · YALE UNIVERSITY · PI DUMAN, RONALD S. · 2005 to 2014
$3.5M
NIMH NIH HHS R01 MH093897NIMH NIH HHS R37 MH045481
6 · The paper itself

Abstract

Dendritic spines provide a compartment for assembly and functional organization of synaptic machinery that plays a fundamental role in neuronal communication and neuroplasticity. Studies in humans as well as in animal models have demonstrated abnormal spine architecture in several psychiatric disorders, including depression and other stress-related illnesses. The negative impact of stress on the density and organization of spines is thought to contribute to the behavioral deficits caused by stress exposure. Moreover, there is now evidence that medication-induced recovery involves changes in synaptic plasticity and dendrite morphology, including increased expression of pre- and postsynaptic plasticity-related proteins, as well as the density and function of axo-spinous synapses. Here we review the evidence from brain imaging and postmortem studies demonstrating that depression is accompanied by structural and functional alterations of cortical and limbic brain regions, including the prefrontal cortex, hippocampus and amygdala. In addition, we present more direct evidence from basic research studies that exposure to stress alters spine morphology, function and plasticity and that antidepressants, particularly new rapid acting agents, reverse these effects. Elucidation of the signaling pathways and molecular mechanisms that control spine synapse assembly and plasticity will contribute to a better understanding of the pathophysiology of depression and development of novel, more effective therapeutic agents.

Indexed as

Neuronal PlasticityStress, PhysiologicalAnimalsBrainBrain-Derived Neurotrophic FactorDepressionHumansNeuronsSynapsesBrain-Derived Neurotrophic FactorACdantidepressantBDBDNFbipolar disorderbrain-derived neurotrophic factorcAMP response element-binding proteinchronic restraint stresschronic unpredictable stressCREBCRSCUSdorsal anterior cingulateECSelectroconvulsive seizureERKextracellular-signal-regulated kinasefMRIforced swim testFSTfunctional magnetic resonance imagingglutamatehippocampusHPAhypothalamic–pituitary–adrenalIESILinescapable stressinfralimbiclearned helplessnessLHlong-term depressionlong-term potentiationLTDLTPmagnetic resonance imagingmajor depressive disordermammalian target of rapamycinMAOIMAPK-phosphatase 1maternal separationMDDmedial prefrontal cortexMKP-1monoamine oxidase inhibitormPFCMRIMSmTORneurotrophic factorNMDAN-methyl-d-aspartate glutamate receptorOFCorbitofrontal cortexposttraumatic stress disorderprefrontal cortexprenatal stressPSPTSDselective serotonin re-uptake inhibitorSSRIstress

Identifiers

PMID23036622
PMCPMC3566360

What OpenQuestion holds

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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.