Evidence map›Paper›PMID 28761082›Full record

ArticleMolecular psychiatry2018

Selective activation of parvalbumin interneurons prevents stress-induced synapse loss and perceptual defects.

C-C Chen, J Lu, R Yang, J B Ding, Y Zuo

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.7field-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

65 citing papers in PubMed, 109 citations in OpenAlex.

  1. Parvalbumin interneurons under stress: converging mechanisms of vulnerability.The international journal of neuropsychopharmacology · 2026
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5 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

5 authors at 2 institutions in 1 country.

C-C ChenDepartment of Molecular, Cell and Developmental Biology, University of California, Santa Cruz, CA, USA.
J LuDepartment of Molecular, Cell and Developmental Biology, University of California, Santa Cruz, CA, USA.
R YangDepartment of Neurosurgery, Stanford University School of Medicine, Palo Alto, CA, USA.
J B DingDepartment of Neurosurgery, Stanford University School of Medicine, Palo Alto, CA, USA.
Y ZuoDepartment of Molecular, Cell and Developmental Biology, University of California, Santa Cruz, CA, USA. yizuo@ucsc.edu.
University of California, Santa Cruz · USStanford University · US

Funding

Dopamine modulation of synaptic plasticity and integration in the striatumR01NS091144 · NINDS · STANFORD UNIVERSITY · PI Jun Ding · 2015 to 2026
$4.2M
Dynamics and molecular mechanism of synaptic connectivity change during learningR01MH104227 · NIMH · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI ZUO, YI · 2014 to 2018
$2.1M
Contribution of astrocytes to the Fragile X SyndromeR01MH109475 · NIMH · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI ZUO, YI · 2016 to 2020
$2.0M
Neurovascular Mechanisms of Time-Dependencies in Stroke RehabilitationR01NS078791 · NINDS · UNIVERSITY OF TEXAS AT AUSTIN · PI DUNN, ANDREW K, JONES, THERESA A · 2012 to 2016
$1.7M
NIMH NIH HHS R01 MH104227NIMH NIH HHS R01 MH109475NINDS NIH HHS R01 NS078791NINDS NIH HHS R01 NS091144
6 · The paper itself

Abstract

Stress, a prevalent experience in modern society, is a major risk factor for many psychiatric disorders. Although sensorimotor abnormalities are often present in these disorders, little is known about how stress affects the sensory cortex. Combining behavioral analyses with in vivo synaptic imaging, we show that stressful experiences lead to progressive, clustered loss of dendritic spines along the apical dendrites of layer (L) 5 pyramidal neurons (PNs) in the mouse barrel cortex, and such spine loss closely associates with deteriorated performance in a whisker-dependent texture discrimination task. Furthermore, the activity of parvalbumin-expressing inhibitory interneurons (PV+ INs) decreases in the stressed mouse due to reduced excitability of these neurons. Importantly, both behavioral defects and structural changes of L5 PNs are prevented by selective pharmacogenetic activation of PV+INs in the barrel cortex during stress. Finally, stressed mice raised under environmental enrichment (EE) maintain normal activation of PV+ INs, normal texture discrimination, and L5 PN spine dynamics similar to unstressed EE mice. Our findings suggest that the PV+ inhibitory circuit is crucial for normal synaptic dynamics in the mouse barrel cortex and sensory function. Pharmacological, pharmacogenetic and environmental approaches to prevent stress-induced maladaptive behaviors and synaptic malfunctions converge on the regulation of PV+ IN activity, pointing to a potential therapeutic target for stress-related disorders.

Indexed as

AnimalsCerebral CortexDendritesDendritic SpinesFemaleInterneuronsMaleMiceMice, Inbred C57BLNeuronsParvalbuminsPyramidal CellsSchizophreniaSignal TransductionStress, PsychologicalSynapsesParvalbumins

Identifiers

PMID28761082
PMCPMC5794672
OpenAlexW2741036834

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.