Evidence map›Paper›PMID 25742132›Full record

ArticlePloS one2015

Presynaptic plasticity as a hallmark of rat stress susceptibility and antidepressant response.

Jose Luis Nieto-Gonzalez, Mai Marie Holm, Irina Vardya, Trine Christensen, Ove Wiborg, Kimmo Jensen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Parvalbumin interneurons under stress: converging mechanisms of vulnerability.The international journal of neuropsychopharmacology · 2026
    Review
  2. Article
  3. Article
  4. The Role of Glutamate Underlying Treatment-resistant Depression.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Making Sense of Rodent Models of Anhedonia.The international journal of neuropsychopharmacology · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Review
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

6 authors at 2 institutions in 2 countries.

Jose Luis Nieto-GonzalezSynaptic Physiology Laboratory, Department of Biomedicine, Building 1160, Aarhus University, DK-8000, Aarhus C, Denmark.
Mai Marie HolmSynaptic Physiology Laboratory, Department of Biomedicine, Building 1160, Aarhus University, DK-8000, Aarhus C, Denmark.
Irina VardyaSynaptic Physiology Laboratory, Department of Biomedicine, Building 1160, Aarhus University, DK-8000, Aarhus C, Denmark.
Trine ChristensenTranslational Neuropsychiatry Unit, Aarhus University Hospital, DK-8240, Risskov, Denmark.
Ove WiborgTranslational Neuropsychiatry Unit, Aarhus University Hospital, DK-8240, Risskov, Denmark.
Kimmo JensenSynaptic Physiology Laboratory, Department of Biomedicine, Building 1160, Aarhus University, DK-8000, Aarhus C, Denmark; Translational Neuropsychiatry Unit, Aarhus University Hospital, DK-8240, Risskov, Denmark; Institute of Neuroscience and Physiology, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.
Aarhus University · DKAarhus University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two main questions are important for understanding and treating affective disorders: why are certain individuals susceptible or resilient to stress, and what are the features of treatment response and resistance? To address these questions, we used a chronic mild stress (CMS) rat model of depression. When exposed to stress, a fraction of rats develops anhedonic-like behavior, a core symptom of major depression, while another subgroup of rats is resilient to CMS. Furthermore, the anhedonic-like state is reversed in about half the animals in response to chronic escitalopram treatment (responders), while the remaining animals are resistant (non-responder animals). Electrophysiology in hippocampal brain slices was used to identify a synaptic hallmark characterizing these groups of animals. Presynaptic properties were investigated at GABAergic synapses onto single dentate gyrus granule cells. Stress-susceptible rats displayed a reduced probability of GABA release judged by an altered paired-pulse ratio of evoked inhibitory postsynaptic currents (IPSCs) (1.48 ± 0.25) compared with control (0.81 ± 0.05) and stress-resilient rats (0.78 ± 0.03). Spontaneous IPSCs (sIPSCs) occurred less frequently in stress-susceptible rats compared with control and resilient rats. Finally, a subset of stress-susceptible rats responding to selective serotonin reuptake inhibitor (SSRI) treatment showed a normalization of the paired-pulse ratio (0.73 ± 0.06) whereas non-responder rats showed no normalization (1.2 ± 0.2). No changes in the number of parvalbumin-positive interneurons were observed. Thus, we provide evidence for a distinct GABAergic synaptopathy which associates closely with stress-susceptibility and treatment-resistance in an animal model of depression.

Indexed as

Neuronal PlasticityAnimalsDepressiongamma-Aminobutyric AcidMaleRatsRats, WistarSynapsesgamma-Aminobutyric Acid

Identifiers

PMID25742132
PMCPMC4350919
OpenAlexW2063976356

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.