Evidence map›Paper›PMID 34362940›Full record

ArticleScientific reports2021

Elimination of glutamatergic transmission from Hb9 interneurons does not impact treadmill locomotion.

Lina M Koronfel, Kevin C Kanning, Angelita Alcos, Christopher E Henderson, Robert M Brownstone

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Excitatory Spinal Lhx9-Derived Interneurons Modulate Locomotor Frequency in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
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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

5 authors at 3 institutions in 4 countries.

Lina M Koronfel *Department of Medical Neuroscience, Faculty of Medicine, Dalhousie University, Halifax, NS, B3H 4R2, Canada.
Kevin C Kanning *Center for Motor Neuron Biology and Disease, Columbia Stem Cell Initiative, Columbia Translational Neuroscience Initiative, Columbia University, New York, NY, 10032, USA.
Angelita Alcos *Department of Medical Neuroscience, Faculty of Medicine, Dalhousie University, Halifax, NS, B3H 4R2, Canada.
Christopher E HendersonCenter for Motor Neuron Biology and Disease, Columbia Stem Cell Initiative, Columbia Translational Neuroscience Initiative, Columbia University, New York, NY, 10032, USA.
Robert M BrownstoneDepartment of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, UCL, London, WC1N 3BG, UK. R.Brownstone@ucl.ac.uk.
Columbia University · USDalhousie University · CAUniversity College London · GB

Funding

Role of Fas death receptor signaling in motor neuron degenerationR01NS056422 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HENDERSON, CHRISTOPHER · 2007 to 2011
$2.0M
Genetic Analysis of Fas in Motor Neuron Cell DeathF32NS055547 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KANNING, KEVIN CHRISTOPHER · 2006 to 2008
$139k
NINDS NIH HHS F32 NS055547NINDS NIH HHS R01 NS056422Wellcome Trust 110193Wellcome Trust 110193/Z/15/Z
6 · The paper itself

Abstract

The spinal cord contains neural circuits that can produce the rhythm and pattern of locomotor activity. It has previously been postulated that a population of glutamatergic neurons, termed Hb9 interneurons, contributes to locomotor rhythmogenesis. These neurons were identified by their expression of the homeobox gene, Hb9, which is also expressed in motor neurons. We developed a mouse line in which Cre recombinase activity is inducible in neurons expressing Hb9. We then used this line to eliminate vesicular glutamate transporter 2 from Hb9 interneurons, and found that there were no deficits in treadmill locomotion. We conclude that glutamatergic neurotransmission by Hb9 interneurons is not required for locomotor behaviour. The role of these neurons in neural circuits remains elusive.

Indexed as

LocomotionPhysical Conditioning, AnimalSynaptic TransmissionAnimalsFemaleGaitGlutamatesHomeodomain ProteinsInterneuronsMaleMiceMice, TransgenicSynapsesTranscription FactorsVesicular Glutamate Transport Protein 2GlutamatesHb9 protein, mouseHomeodomain ProteinsSlc17a6 protein, mouseTranscription FactorsVesicular Glutamate Transport Protein 2

Identifiers

PMID34362940
PMCPMC8346588
OpenAlexW3123262423

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.