Evidence map›Paper›PMID 40739884›Full record

ArticleJournal of neurochemistry2025

MGlu5 Dependent Mitochondrial Translocation of PKCδ: A Mechanism Raising Astrocytic Oxidative Metabolism in Response to Extracellular Glutamate.

Kiavasch M N Farid, Rodrigo Lerchundi, Christine R Rose, Amin Derouiche

Abstract read
In one paragraph

Article in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

  1. Review
  2. 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

4 authors.

Kiavasch M N FaridInstitute of Anatomy II, Goethe University Frankfurt, Frankfurt am Main, Germany.
Rodrigo LerchundiInstitute of Neurobiology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Christine R RoseInstitute of Neurobiology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Amin DerouicheInstitute of Anatomy II, Goethe University Frankfurt, Frankfurt am Main, Germany.ORCID https://orcid.org/0000-0002-7309-2044

Funding

Deutsche Forschungsgemeinschaft Ro2327/13-2Deutsche Forschungsgemeinschaft Ro2327/8-2Deutsche Forschungsgemeinschaft RU2795 "Synapses under stress"Deutsche Forschungsgemeinschaft SPP 1757 "Glial Heterogeneity"
6 · The paper itself

Abstract

Synaptic activity imposes high demands of local energy production on astrocytes. However, the (an)aerobic pathways and fuel for generation of energy equivalents in astrocytes are still debated. Also, mechanisms to ensure rapid metabolic adaptation to bouts of neuronal activity have not been sufficiently explored. Here, we show a mechanism in astrocytes linking extracellular glutamate to upregulation of oxidative phosphorylation. We stimulated primary astrocytes with glutamate, and applied fluorescent immunocytochemistry with anti-protein kinase Cδ (PKCδ), anti-pyruvate dehydrogenase (PDH) and anti-phospho-PDH antibodies, and object oriented image analysis. Glutamate induces mitochondrial translocation of PKCδ and subsequent activation of the mitochondrial enzyme PDH-the point-of-no-return in the utilization of carbohydrates. Using the specific mGlu5 antagonist 2-Methyl-6-(phenylethynyl)pyridine hydrochloride (MPEP), the metabotropic glutamate receptor 5 (mGlu5) was identified as the key receptor inducing mitochondrial PKCδ translocation and PDH activation. We demonstrate by luminometric ATP assay and subtype-specific inhibitors of PKC and mGlu5 that the distinct initial drop in intracellular ATP following glutamate application is counteracted by the mGlu5/PKCδ-dependent mitochondrial activation. mGlu5 inhibition decreases ATP production also in astrocytes in the acute brain slice. Collectively, these findings reveal that astrocytes possess a potential for oxidative phosphorylation that can be stimulated by extracellular glutamate and the mGlu5/PKCδ/PDH axis, suggesting targets for pathologies involving excess glutamate. This also focuses the issue of activity-induced glia-neuronal metabolic interaction on perisynaptic energetics and the glia-synaptic microenvironment. Up-regulation of astrocytic metabolism via the mGlu5/PKCδ/PDH axis may affect only those perisynaptic astrocyte processes (PAPs) close to the active synapse(s), leaving other astrocyte domains and the whole cell unchanged.

Indexed as

AstrocytesGlutamic AcidMitochondriaProtein Kinase C-deltaReceptor, Metabotropic Glutamate 5AnimalsCells, CulturedMiceMice, Inbred C57BLOxidative PhosphorylationProtein TransportRatsGlutamic AcidProtein Kinase C-deltaReceptor, Metabotropic Glutamate 5glia‐synaptic interactionneurometabolic couplingpyruvate dehydrogenasepyruvate dehydrogenase phosphatasetripartite synapse

Identifiers

PMID40739884
PMCPMC12311410

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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.