Evidence map›Paper›PMID 25873863›Full record

ArticleFrontiers in cellular neuroscience2015

Defective microglial development in the hippocampus of Cx3cr1 deficient mice.

Francesca Pagani, Rosa C Paolicelli, Emanuele Murana, Barbara Cortese, Silvia Di Angelantonio, Emanuele Zurolo, Eva Guiducci, Tiago A Ferreira, Stefano Garofalo, Myriam Catalano and 7 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 91 citations in OpenAlex.

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  14. Microglial Regulation of Sleep and Wakefulness.Advances in neurobiology · 2024
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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

17 authors at 8 institutions in 3 countries.

Francesca PaganiCenter for Life Nanoscience - Istituto Italiano di Tecnologia@Sapienza, Rome Italy.
Rosa C PaolicelliDivision of Psychiatry Research, University of Zürich, Zürich Switzerland ; Mouse Biology Unit, European Molecular Biology Laboratory, Monterotondo Italy.
Emanuele MuranaDepartment of Physiology and Pharmacology, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome Italy.
Barbara CorteseConsiglio Nazionale delle Ricerche - Institute of Inorganic Methodologies and Plasmas, Department of Physics, Sapienza University of Rome, Rome Italy.
Silvia Di AngelantonioCenter for Life Nanoscience - Istituto Italiano di Tecnologia@Sapienza, Rome Italy ; Department of Physiology and Pharmacology, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome Italy.
Emanuele ZuroloDepartment of Neuropathology, Academic Medical Center, University of Amsterdam Amsterdam, Netherlands.
Eva GuiducciMouse Biology Unit, European Molecular Biology Laboratory, Monterotondo Italy.
Tiago A FerreiraMouse Biology Unit, European Molecular Biology Laboratory, Monterotondo Italy.
Stefano GarofaloDepartment of Physiology and Pharmacology, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome Italy.
Myriam CatalanoDepartment of Physiology and Pharmacology, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome Italy ; Istituto di Ricovero e Cura a Carattere Scientifico Neuromed Pozzilli, Italy.
Giuseppina D'AlessandroDepartment of Physiology and Pharmacology, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome Italy ; Istituto di Ricovero e Cura a Carattere Scientifico Neuromed Pozzilli, Italy.
Alessandra PorziaDepartment of Molecular Medicine, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome Rome, Italy.
Giovanna PeruzziCenter for Life Nanoscience - Istituto Italiano di Tecnologia@Sapienza, Rome Italy.
Fabrizio MainieroDepartment of Experimental Medicine, Sapienza University of Rome Rome, Italy.
Cristina LimatolaDepartment of Physiology and Pharmacology, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome Italy ; Istituto di Ricovero e Cura a Carattere Scientifico Neuromed Pozzilli, Italy.
Cornelius T GrossMouse Biology Unit, European Molecular Biology Laboratory, Monterotondo Italy.
Davide RagozzinoDepartment of Physiology and Pharmacology, Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome Italy ; Istituto di Ricovero e Cura a Carattere Scientifico Neuromed Pozzilli, Italy.
Istituto Pasteur · ITEuropean Molecular Biology Laboratory · ITSapienza University of Rome · ITIstituto Neurologico Mediterraneo · ITItalian Institute of Technology · ITAcademic Medical Center · NLInstitute of Inorganic Methodologies and Plasmas · ITUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglial cells participate in brain development and influence neuronal loss and synaptic maturation. Fractalkine is an important neuronal chemokine whose expression increases during development and that can influence microglia function via the fractalkine receptor, CX3CR1. Mice lacking Cx3cr1 show a variety of neuronal defects thought to be the result of deficient microglia function. Activation of CX3CR1 is important for the proper migration of microglia to sites of injury and into the brain during development. However, little is known about how fractalkine modulates microglial properties during development. Here we examined microglial morphology, response to ATP, and K(+) current properties in acute brain slices from Cx3cr1 knockout mice across postnatal hippocampal development. We found that fractalkine signaling is necessary for the development of several morphological and physiological features of microglia. Specifically, we found that the occurrence of an outward rectifying K(+) current, typical of activated microglia, that peaked during the second and third postnatal week, was reduced in Cx3cr1 knockout mice. Fractalkine signaling also influenced microglial morphology and ability to extend processes in response to ATP following its focal application to the slice. Our results reveal the developmental profile of several morphological and physiological properties of microglia and demonstrate that these processes are modulated by fractalkine signaling.

Indexed as

CX3CR1developmentfractalkinemicrogliapotassium currentsrearrangement

Identifiers

PMID25873863
PMCPMC4379915
OpenAlexW2018686878

What OpenQuestion holds

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Registered trials

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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.