Evidence map›Paper›PMID 32976803›Full record

ArticleCurrent biology : CB2020

Hypothalamic Pomc Neurons Innervate the Spinal Cord and Modulate the Excitability of Premotor Circuits.

Philip Reinoß, Elisa Ciglieri, Marielle Minére, Stephan Bremser, Andreas Klein, Heiko Löhr, Patrick M Fuller, Ansgar Büschges, Peter Kloppenburg, Henning Fenselau and 1 more

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In one paragraph

Article in Current biology : CB, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

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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

11 authors at 5 institutions in 2 countries.

Philip ReinoßInstitute for Zoology, University of Cologne, Zülpicher Straße 47b, Cologne 50674, Germany.
Elisa CiglieriSynaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Straße 50, Cologne 50931, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Straße 26, Cologne 50924, Germany.
Marielle MinéreSynaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Straße 50, Cologne 50931, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Straße 26, Cologne 50924, Germany.
Stephan BremserInstitute for Zoology, University of Cologne, Zülpicher Straße 47b, Cologne 50674, Germany; Synaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Straße 50, Cologne 50931, Germany.
Andreas KleinInstitute for Zoology, University of Cologne, Zülpicher Straße 47b, Cologne 50674, Germany.
Heiko LöhrInstitute for Zoology, University of Cologne, Zülpicher Straße 47b, Cologne 50674, Germany.
Patrick M FullerDepartment of Neurology, Beth Israel Deaconess Medical Center and Division of Sleep Medicine, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA.
Ansgar BüschgesInstitute for Zoology, University of Cologne, Zülpicher Straße 47b, Cologne 50674, Germany.
Peter KloppenburgInstitute for Zoology, University of Cologne, Zülpicher Straße 47b, Cologne 50674, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Joseph-Stelzmann-Straße 26, Cologne 50931, Germany.
Henning FenselauSynaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Straße 50, Cologne 50931, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Straße 26, Cologne 50924, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Joseph-Stelzmann-Straße 26, Cologne 50931, Germany. Electronic address: henning.fenselau@sf.mpg.de.
Matthias HammerschmidtInstitute for Zoology, University of Cologne, Zülpicher Straße 47b, Cologne 50674, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Joseph-Stelzmann-Straße 26, Cologne 50931, Germany; Center for Molecular Medicine Cologne, University of Cologne, Robert-Koch-Straße 21, Cologne 50931, Germany. Electronic address: mhammers@uni-koeln.de.
University of Cologne · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEMax Planck Institute for Metabolism Research · DEHarvard University · USUniversity Hospital Cologne · DE

Funding

Systematic Vertebrate Functional GenomicsR01GM063904 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI EKKER, STEPHEN CARL · 2001 to 2025
$10.7M
Systematic Vertebrate Functional GenomicsR56GM063904 · NIGMS · MAYO CLINIC ROCHESTER · PI EKKER, STEPHEN CARL · 2009 to 2010
$611k
NIGMS NIH HHS R01 GM063904NIGMS NIH HHS R56 GM063904
6 · The paper itself

Abstract

Locomotion requires energy, yet animals need to increase locomotion in order to find and consume food in energy-deprived states. While such energy homeostatic coordination suggests brain origin, whether the central melanocortin 4 receptor (Mc4r) system directly modulates locomotion through motor circuits is unknown. Here, we report that hypothalamic Pomc neurons in zebrafish and mice have long-range projections into spinal cord regions harboring Mc4r-expressing V2a interneurons, crucial components of the premotor networks. Furthermore, in zebrafish, Mc4r activation decreases the excitability of spinal V2a neurons as well as swimming and foraging, while systemic or V2a neuron-specific blockage of Mc4r promotes locomotion. In contrast, in mice, electrophysiological recordings revealed that two-thirds of V2a neurons in lamina X are excited by the Mc4r agonist α-MSH, and acute inhibition of Mc4r signaling reduces locomotor activity. In addition, we found other Mc4r neurons in spinal lamina X that are inhibited by α-MSH, which is in line with previous studies in rodents where Mc4r agonists reduced locomotor activity. Collectively, our studies identify spinal V2a interneurons as evolutionary conserved second-order neurons of the central Mc4r system, providing a direct anatomical and functional link between energy homeostasis and locomotor control systems. The net effects of this modulatory system on locomotor activity can vary between different vertebrate species and, possibly, even within one species. We discuss the biological sense of this phenomenon in light of the ambiguity of locomotion on energy balance and the different living conditions of the different species.

Indexed as

AnimalsAnimals, Genetically ModifiedArcuate Nucleus of HypothalamusBiological EvolutionElectrophysiological PhenomenaInterneuronsLocomotionMiceModels, AnimalNerve NetPro-OpiomelanocortinReceptor, Melanocortin, Type 4Signal TransductionSpinal CordZebrafishZebrafish ProteinsMC4R protein, mousemc4r protein, zebrafishpomca protein, zebrafishPro-OpiomelanocortinReceptor, Melanocortin, Type 4Zebrafish ProteinsAgrpenergy homeostasisinterneuronslocomotionMc4rmouseneurocircuitPomcspinal cordzebrafish

Identifiers

PMID32976803
PMCPMC8847999
OpenAlexW3087959751

What OpenQuestion holds

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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.