Evidence map›Paper›PMID 38443593›Full record

ArticleNature metabolism2024

Neuron-astrocyte metabolic coupling facilitates spinal plasticity and maintenance of inflammatory pain.

Sebastián Marty-Lombardi, Shiying Lu, Wojciech Ambroziak, Katrin Schrenk-Siemens, Jialin Wang, Anna A DePaoli-Roach, Anna M Hagenston, Hagen Wende, Anke Tappe-Theodor, Manuela Simonetti and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Nature metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

33 citing papers in PubMed, 30 citations in OpenAlex.

  1. Glial cells in neuropathic pain.Physiological reviews · 2026
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  9. Cell-specific isotope labeling identifiesbioRxiv : the preprint server for biology · 2026
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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

15 authors at 3 institutions in 2 countries.

Sebastián Marty-Lombardi *Institute of Pharmacology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-8309-9875
Shiying Lu *Institute of Pharmacology, Heidelberg University, Heidelberg, Germany.
Wojciech AmbroziakInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-3801-5908
Katrin Schrenk-SiemensInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-8297-4399
Jialin WangInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0003-3026-6507
Anna A DePaoli-RoachDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Anna M HagenstonDepartment of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-7747-5336
Hagen WendeInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany.
Anke Tappe-TheodorInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany.
Manuela SimonettiInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0003-0056-7595
Hilmar BadingDepartment of Neurobiology, Interdisciplinary Center for Neurosciences (IZN), Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0003-0258-4348
Jürgen G OkunDietmar-Hopp-Metabolic Center, Division of Neuropaediatrics and Metabolic Medicine, Heidelberg University, Heidelberg, Germany.
Rohini KunerInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-3333-9129
Thomas FlemingDepartment of Endocrinology, Diabetology, Metabolism and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-3232-4515
Jan SiemensInstitute of Pharmacology, Heidelberg University, Heidelberg, Germany. jan.siemens@pharma.uni-heidelberg.de.ORCID http://orcid.org/0000-0001-9051-9217
Heidelberg University · DEEuropean Molecular Biology Organization · DEIndiana University School of Medicine

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1158European Commission (EC) ERC-CoG-772395Human Frontier Science Program (HFSP) LT000762/2019-L
6 · The paper itself

Abstract

Long-lasting pain stimuli can trigger maladaptive changes in the spinal cord, reminiscent of plasticity associated with memory formation. Metabolic coupling between astrocytes and neurons has been implicated in neuronal plasticity and memory formation in the central nervous system, but neither its involvement in pathological pain nor in spinal plasticity has been tested. Here we report a form of neuroglia signalling involving spinal astrocytic glycogen dynamics triggered by persistent noxious stimulation via upregulation of the Protein Targeting to Glycogen (PTG) in spinal astrocytes. PTG drove glycogen build-up in astrocytes, and blunting glycogen accumulation and turnover by Ptg gene deletion reduced pain-related behaviours and promoted faster recovery by shortening pain maintenance in mice. Furthermore, mechanistic analyses revealed that glycogen dynamics is a critically required process for maintenance of pain by facilitating neuronal plasticity in spinal lamina 1 neurons. In summary, our study describes a previously unappreciated mechanism of astrocyte-neuron metabolic communication through glycogen breakdown in the spinal cord that fuels spinal neuron hyperexcitability.

Indexed as

AstrocytesPainAnimalsGlycogenMiceNeuronsSpinal CordGlycogen

Identifiers

PMID38443593
PMCPMC10963271
OpenAlexW4392460448

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.