Evidence map›Paper›PMID 24342992›Full record

ArticleMolecular psychiatry2014

Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis.

T Kreisel, M G Frank, T Licht, R Reshef, O Ben-Menachem-Zidon, M V Baratta, S F Maier, R Yirmiya

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 329 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
329citing papers in PubMed, 1 pooled it
22.9field-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

329 citing papers in PubMed, 1 synthesis or guideline pooled it, 665 citations in OpenAlex.

  1. Pooled it
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  8. International journal of molecular sciences · 2026
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269 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

8 authors at 2 institutions in 2 countries.

T KreiselDepartment of Psychology, The Hebrew University of Jerusalem, Jerusalem, Israel.
M G FrankDepartment of Psychology and Neuroscience, University of Colorado, Boulder, CO, USA.
T LichtDeparment of Developmental Biology and Cancer Research, Hebrew University Hadassah Medical School, Jerusalem, Israel.
R ReshefDepartment of Psychology, The Hebrew University of Jerusalem, Jerusalem, Israel.
O Ben-Menachem-ZidonDepartment of Psychology, The Hebrew University of Jerusalem, Jerusalem, Israel.
M V BarattaDepartment of Psychology and Neuroscience, University of Colorado, Boulder, CO, USA.
S F MaierDepartment of Psychology and Neuroscience, University of Colorado, Boulder, CO, USA.
R YirmiyaDepartment of Psychology, The Hebrew University of Jerusalem, Jerusalem, Israel.
Hebrew University of Jerusalem · ILUniversity of Colorado Boulder · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The limited success in understanding the pathophysiology of major depression may result from excessive focus on the dysfunctioning of neurons, as compared with other types of brain cells. Therefore, we examined the role of dynamic alterations in microglia activation status in the development of chronic unpredictable stress (CUS)-induced depressive-like condition in rodents. We report that following an initial period (2-3 days) of stress-induced microglial proliferation and activation, some microglia underwent apoptosis, leading to reductions in their numbers within the hippocampus, but not in other brain regions, following 5 weeks of CUS exposure. At that time, microglia displayed reduced expression of activation markers as well as dystrophic morphology. Blockade of the initial stress-induced microglial activation by minocycline or by transgenic interleukin-1 receptor antagonist overexpression rescued the subsequent microglial apoptosis and decline, as well as the CUS-induced depressive-like behavior and suppressed neurogenesis. Similarly, the antidepressant drug imipramine blocked the initial stress-induced microglial activation as well as the CUS-induced microglial decline and depressive-like behavior. Treatment of CUS-exposed mice with either endotoxin, macrophage colony-stimulating factor or granulocyte-macrophage colony-stimulating factor, all of which stimulated hippocampal microglial proliferation, partially or completely reversed the depressive-like behavior and dramatically increased hippocampal neurogenesis, whereas treatment with imipramine or minocycline had minimal or no anti-depressive effects, respectively, in these mice. These findings provide direct causal evidence that disturbances in microglial functioning has an etiological role in chronic stress-induced depression, suggesting that microglia stimulators could serve as fast-acting anti-depressants in some forms of depressive and stress-related conditions.

Indexed as

AnimalsApoptosisBehavior, AnimalBrainCell ProliferationChronic DiseaseDepressive DisorderHippocampusMaleMiceMice, TransgenicMicrogliaNeurogenesisRatsStress, PsychologicalUncertainty

Identifiers

PMID24342992
OpenAlexW2051359369

What OpenQuestion holds

Textmetadata
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.