Evidence map›Paper›PMID 15099689›Full record

ArticleNeuroscience2004

Chronic stress enhances ibotenic acid-induced damage selectively within the hippocampal CA3 region of male, but not female rats.

C D Conrad, J L Jackson, L S Wise

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 60 citations in OpenAlex.

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  16. Amphetamine toxicities: classical and emerging mechanisms.Annals of the New York Academy of Sciences · 2010
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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 1 institution in 1 country.

C D ConradDepartment of Psychology, Box 1104, Arizona State University, Tempe, AZ 85287-1104, USA. conradc@asu.edu
J L Jackson
L S Wise
Arizona State University · US

Funding

Significance of Stress-Induced Hippocampal AtrophyR01MH064727 · NIMH · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI CONRAD, CHERYL D · 2002 to 2006
$1.0M
NIMH NIH HHS MH64727NIMH NIH HHS R01 MH064727
6 · The paper itself

Abstract

The purpose of this investigation was to assess the ability of the hippocampus to withstand a metabolic challenge following chronic stress. An N-methyl-d-aspartate receptor excitotoxin (ibotenic acid, IBO) was infused into the CA3 region of the hippocampus following a period of restraint for 6 h/day/21 days. Following the end of restraint when CA3 dendritic retraction persists (3 to 4 days), rats were infused with IBO (or vehicle) into the CA3 region of the hippocampus. Stressed male rats showed significantly more CA3 damage after IBO infusion relative to controls and the saline-infused side. Moreover, IBO-exacerbation of damage in males was not observed in the CA3 region 3 to 4 days after acute stress (6 h restraint), nor in the CA1 region after chronic stress. Females were also examined and chronic stress did not exacerbate IBO damage in the CA3 region. Overall, these results demonstrate that chronic stress compromises the ability of the hippocampus to withstand a metabolic challenge days after the chronic stress regimen has subsided in male rats. Whether the conditions surrounding CA3 dendritic retraction in females represents vulnerability is less clear and warrants further investigation.

Indexed as

Sex CharacteristicsAcute DiseaseAnimalsChronic DiseaseFemaleHippocampusIbotenic AcidMaleNerve DegenerationNeuronsNeurotoxinsRatsRats, Sprague-DawleyReaction TimeStress, PhysiologicalIbotenic AcidNeurotoxins

Identifiers

PMID15099689
PMCPMC1360690
OpenAlexW2001242524

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.