Evidence map›Paper›PMID 27353765›Full record

ArticleScientific reports2016

Growth differentiation factor-15 promotes glutamate release in medial prefrontal cortex of mice through upregulation of T-type calcium channels.

Dong-Dong Liu, Jun-Mei Lu, Qian-Ru Zhao, Changlong Hu, Yan-Ai Mei

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. Combined targeting of PRDX6 and GSTP1 as a potential differentiation strategy for neuroblastoma treatment.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  6. Review
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  10. Review
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  13. GDF15, an update of the physiological and pathological roles it plays: a review.Pflugers Archiv : European journal of physiology · 2020
    Review
  14. Article
  15. Article
  16. Calcium dependence of spontaneous neurotransmitter release.Journal of neuroscience research · 2018
    Review
  17. Article
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

5 authors at 2 institutions in 1 country.

Dong-Dong LiuInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China.
Jun-Mei LuInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China.
Qian-Ru ZhaoInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China.
Changlong HuInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China.
Yan-Ai MeiInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology and School of Life Sciences, Fudan University, Shanghai 200433, China.
State Key Laboratory of Medical NeurobiologyFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth differentiation factor-15 (GDF-15) has been implicated in ischemic brain injury and synapse development, but its involvement in modulating neuronal excitability and synaptic transmission remain poorly understood. In this study, we investigated the effects of GDF-15 on non-evoked miniature excitatory post-synaptic currents (mEPSCs) and neurotransmitter release in the medial prefrontal cortex (mPFC) in mice. Incubation of mPFC slices with GDF-15 for 60 min significantly increased the frequency of mEPSCs without effect on their amplitude. GDF-15 also significantly elevated presynaptic glutamate release, as shown by HPLC. These effects were blocked by dual TGF-β type I receptor (TβRI) and TGF-β type II receptor (TβRII) antagonists, but not by a TβRI antagonist alone. Meanwhile, GDF-15 enhanced pERK level, and inhibition of MAPK/ERK activity attenuated the GDF-15-induced increases in mEPSC and glutamate release. Blocking T-type calcium channels reduced the GDF-15 induced up-regulation of synaptic transmission. Membrane-protein extraction and use of an intracellular protein-transport inhibitor showed that GDF-15 promoted CaV3.1 and CaV3.3 α-subunit expression by trafficking to the membrane. These results confirm previous findings in cerebellar granule neurons, in which GDF-15 induces its neurobiological effects via TβRII and activation of the ERK pathway, providing novel insights into the mechanism of GDF-15 function in cortical neurons.

Indexed as

AnimalsCalcium Channels, T-TypeFemaleGlutamic AcidGrowth Differentiation Factor 15MAP Kinase Signaling SystemMicePrefrontal CortexProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IISynaptic TransmissionCacna1g protein, mouseCacna1i protein, mouseCalcium Channels, T-TypeGdf15 protein, mouseGlutamic AcidGrowth Differentiation Factor 15Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type II

Identifiers

PMID27353765
PMCPMC4926092
OpenAlexW2460555735

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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.