Evidence map›Paper›PMID 27721466›Full record

ArticleScientific reports2016

The chemokine CXCL16 modulates neurotransmitter release in hippocampal CA1 area.

Maria Amalia Di Castro, Flavia Trettel, Giampaolo Milior, Laura Maggi, Davide Ragozzino, Cristina Limatola

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-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

29 citing papers in PubMed, 42 citations in OpenAlex.

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  8. An Ascending Excitatory Circuit from the Dorsal Raphe for Sensory Modulation of Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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  17. Article
  18. Microglia: sculptors of neuropathic pain?Royal Society open science · 2020
    Review
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  20. 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 3 institutions in 1 country.

Maria Amalia Di CastroIstituto Pasteur-Italia, Dipartimento di Fisiologia e Farmacologia, Sapienza Università di Roma, Piazzale Aldo Moro 5, 00185 Roma, Italy.
Flavia TrettelIstituto Pasteur-Italia, Dipartimento di Fisiologia e Farmacologia, Sapienza Università di Roma, Piazzale Aldo Moro 5, 00185 Roma, Italy.
Giampaolo MiliorIstituto Pasteur-Italia, Dipartimento di Fisiologia e Farmacologia, Sapienza Università di Roma, Piazzale Aldo Moro 5, 00185 Roma, Italy.
Laura MaggiIstituto Pasteur-Italia, Dipartimento di Fisiologia e Farmacologia, Sapienza Università di Roma, Piazzale Aldo Moro 5, 00185 Roma, Italy.
Davide RagozzinoDipartimento di Fisiologia e Farmacologia, Sapienza Università di Roma, Piazzale Aldo Moro 5, 00185 Roma, Italy.
Cristina LimatolaIstituto Pasteur-Italia, Dipartimento di Fisiologia e Farmacologia, Sapienza Università di Roma, Piazzale Aldo Moro 5, 00185 Roma, Italy.
Sapienza University of Rome · ITIstituto Pasteur · ITIstituto Neurologico Mediterraneo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokines have several physio-pathological roles in the brain. Among them, the modulation of synaptic contacts and neurotransmission recently emerged as crucial activities during brain development, in adulthood, upon neuroinflammation and neurodegenerative diseases. CXCL16 is a chemokine normally expressed in the brain, where it exerts neuroprotective activity against glutamate-induced damages through cross communication with astrocytes and the involvement of the adenosine receptor type 3 (A3R) and the chemokine CCL2. Here we demonstrated for the first time that CXCL16 exerts a modulatory activity on inhibitory and excitatory synaptic transmission in CA1 area. We found that CXCL16 increases the frequency of the miniature inhibitory synaptic currents (mIPSCs) and the paired-pulse ratio (PPR) of evoked IPSCs (eIPSCs), suggesting a presynaptic modulation of the probability of GABA release. In addition, CXCL16 increases the frequency of the miniature excitatory synaptic currents (mEPSCs) and reduces the PPR of evoked excitatory transmission, indicating that the chemokine also modulates and enhances the release of glutamate. These effects were not present in the A3RKO mice and in WT slices treated with minocycline, confirming the involvement of A3 receptors and introducing microglial cells as key mediators of the modulatory activity of CXCL16 on neurons.

Indexed as

AnimalsCA1 Region, HippocampalChemokine CXCL16Evoked PotentialsGlutamic AcidMiceMice, KnockoutMinocyclineNeurotransmitter AgentsReceptor, Adenosine A3Synaptic TransmissionChemokine CXCL16Cxcl16 protein, mouseGlutamic AcidMinocyclineNeurotransmitter AgentsReceptor, Adenosine A3

Identifiers

PMID27721466
PMCPMC5056385
OpenAlexW2530849783

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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.