Evidence map›Paper›PMID 26577396›Full record

ArticleNeurochemical research2016

Experimental Post-traumatic Stress Disorder Decreases Astrocyte Density and Changes Astrocytic Polarity in the CA1 Hippocampus of Male Rats.

Lisiani Saur, Pedro Porto Alegre Baptista, Pamela Brambilla Bagatini, Laura Tartari Neves, Raquel Mattos de Oliveira, Sabrina Pereira Vaz, Kelly Ferreira, Susane Alves Machado, Régis Gemerasca Mestriner, Léder Leal Xavier

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In one paragraph

Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Lisiani SaurLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Pedro Porto Alegre BaptistaLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Pamela Brambilla BagatiniLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Laura Tartari NevesLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Raquel Mattos de OliveiraLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Sabrina Pereira VazLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Kelly FerreiraLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Susane Alves MachadoLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Régis Gemerasca MestrinerLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Léder Leal XavierLaboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil. llxavier@pucrs.br.
Pontifícia Universidade Católica do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-traumatic stress disorder (PTSD) is a psychiatric condition resulting from exposure to a traumatic event. It is characterized by several debilitating symptoms including re-experiencing the past trauma, avoidance behavior, increased fear, and hyperarousal. Key roles in the neuropathology of PTSD and its symptomatology have been attributed to the hippocampus and amygdala. These regions are involved in explicit memory processes and context encoding during fear conditioning. The aim of our study was to investigate whether PTSD is capable of altering the morphology, density and expression of glial fibrillary acidic protein (GFAP) in astrocytes from the CA1 region of the hippocampus and the medial amygdala and correlate the data obtained with the orientation index of the polarity of astrocytes. Thirty male rats were divided in two groups: control (n = 15) and PTSD (n = 15). The inescapable shock protocol, in which the animals are exposed to a single episode of footshock, was used to induce PTSD. Our results show that, in the hippocampus, PTSD is capable of decreasing the density of GFAP+ astrocytes as well as altering astrocytic morphology, as shown by the reductions observed in the total number of primary processes, in the number of primary processes in the lateral quadrants, and the degree of branching in the lateral quadrants. The analysis of the orientation index indicates that PTSD alters the polarity of hippocampal astrocytes. No alterations were observed in the amygdala astrocytes. Therefore, this study demonstrates notable changes in hippocampal astrocytes, supporting the concept that these cells play an important role in PTSD symptomatology.

Indexed as

AnimalsAstrocytesCA1 Region, HippocampalCell CountCell PolarityCorticomedial Nuclear ComplexGlial Fibrillary Acidic ProteinMaleRats, WistarStress Disorders, Post-TraumaticGlial Fibrillary Acidic ProteinAmygdalaAstrocyteGFAPHippocampusMorphologyPTSD

Identifiers

PMID26577396
OpenAlexW2197177898

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.