Evidence map›Paper›PMID 25266126›Full record

ArticleMolecular psychiatry2015

Neuregulin 1 signalling modulates mGluR1 function in mesencephalic dopaminergic neurons.

A Ledonne, A Nobili, E C Latagliata, V Cavallucci, E Guatteo, S Puglisi-Allegra, M D'Amelio, N B Mercuri

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 27% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. ALDH1L1 reverses CD8Journal of translational medicine · 2026
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  13. Cell-Cell Communication AlterationsFrontiers in aging neuroscience · 2022
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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

8 authors at 2 institutions in 1 country.

A Ledonne1] Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy [2] Department of Systems Medicine, University of Rome 'Tor Vergata', Rome, Italy.
A NobiliDepartment of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy.
E C LatagliataDepartment of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy.
V CavallucciDepartment of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy.
E GuatteoDepartment of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy.
S Puglisi-Allegra1] Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy [2] Department of Psychology and 'Daniel Bovet' Center, University of Rome 'La Sapienza', Rome, Italy.
M D'Amelio1] Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy [2] Laboratory of Molecular Neurosciences, Medical School University Campus-Biomedico, Rome, Italy.
N B Mercuri1] Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Rome, Italy [2] Department of Systems Medicine, University of Rome 'Tor Vergata', Rome, Italy.
Fondazione Santa Lucia · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuregulin 1 (NRG1) is a trophic factor that has an essential role in the nervous system by modulating neurodevelopment, neurotransmission and synaptic plasticity. Despite the evidence that NRG1 and its receptors, ErbB tyrosine kinases, are expressed in mesencephalic dopaminergic nuclei and their functional alterations are reported in schizophrenia and Parkinson's disease, the role of NRG1/ErbB signalling in dopaminergic neurons remains unclear. Here we found that NRG1 selectively increases the metabotropic glutamate receptor 1 (mGluR1)-activated currents by inducing synthesis and trafficking to membrane of functional receptors and stimulates phosphatidylinositol 3-kinase-Akt-mammalian target of rapamycin (PI3K-Akt-mTOR) pathway, which is required for mGluR1 function. Notably, an endogenous NRG1/ErbB tone is necessary to maintain mGluR1 function, by preserving its surface membrane expression in dopaminergic neurons. Consequently, it enables striatal mGluR1-induced dopamine outflow in in vivo conditions. Our results identify a novel role of NRG1 in the dopaminergic neurons, whose functional alteration might contribute to devastating diseases, such as schizophrenia and Parkinson's disease.

Indexed as

AnimalsDopamineDopaminergic NeuronsErbB ReceptorsMaleMembrane PotentialsMesencephalonMicrodialysisNeuregulin-1Patch-Clamp TechniquesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRats, WistarReceptors, Metabotropic GlutamateSignal TransductionTissue Culture TechniquesDopamineErbB Receptorsmetabotropic glutamate receptor type 1mTOR protein, ratNeuregulin-1Nrg1 protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Metabotropic GlutamateTOR Serine-Threonine Kinases

Identifiers

PMID25266126
OpenAlexW2128250648

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.