Evidence map›Paper›PMID 26740651›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016

Glycinergic Neurotransmission: A Potent Regulator of Embryonic Motor Neuron Dendritic Morphology and Synaptic Plasticity.

Matthew J Fogarty, Refik Kanjhan, Mark C Bellingham, Peter G Noakes

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review of the Pathology of Muscle in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Postnatal survival of phrenic motor neurons is promoted by BDNF/TrkB.FL signaling.Journal of applied physiology (Bethesda, Md. : 1985) · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Inhibitory Synaptic Influences on Developmental Motor Disorders.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Tongue muscle contractile, fatigue, and fiber type properties in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2021
    Article
  17. Article
  18. Impact of congenital diaphragmatic hernia on diaphragm muscle function in neonatal rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2021
    Article
  19. Article
  20. Review
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 at 2 institutions in 2 countries.

Matthew J FogartySchool of Biomedical Sciences and.
Refik KanjhanSchool of Biomedical Sciences and.ORCID http://orcid.org/0000-0003-2933-5034
Mark C BellinghamSchool of Biomedical Sciences and.
Peter G NoakesSchool of Biomedical Sciences and Queensland Brain Institute, University of Queensland, St. Lucia, 4072 Queensland, Australia p.noakes@uq.edu.au.
Institute of Biomedical Science · GBThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence suggests that central synaptic inputs onto motor neurons (MNs) play an important role in developmental regulation of the final number of MNs and their muscle innervation for a particular motor pool. Here, we describe the effect of genetic deletion of glycinergic neurotransmission on single MN structure and on functional excitatory and inhibitory inputs to MNs. We measured synaptic currents in E18.5 hypoglossal MNs from brain slices using whole-cell patch-clamp recording, followed by dye-filling these same cells with Neurobiotin, to define their morphology by high-resolution confocal imaging and 3D reconstruction. We show that hypoglossal MNs of mice lacking gephyrin display increased dendritic arbor length and branching, increased spiny processes, decreased inhibitory neurotransmission, and increased excitatory neurotransmission. These findings suggest that central glycinergic synaptic activity plays a vital role in regulating MN morphology and glutamatergic central synaptic inputs during late embryonic development. SIGNIFICANCE STATEMENT: MNs within the brainstem and spinal cord are responsible for integrating a diverse array of synaptic inputs into discrete contractions of skeletal muscle to achieve coordinated behaviors, such as breathing, vocalization, and locomotion. The last trimester in utero is critical in neuromotor development, as this is when central and peripheral synaptic connections are made onto and from MNs. At this time-point, using transgenic mice with negligible glycinergic postsynaptic responses, we show that this deficiency leads to abnormally high excitatory neurotransmission and alters the dendritic architecture responsible for coherently integrating these inputs. This study compliments the emerging concept that neurodevelopmental disorders (including autism, epilepsy, and amyotrophic lateral sclerosis) are underpinned by synaptic dysfunction and therefore will be useful to neuroscientists and neurologists alike.

Indexed as

AnimalsCells, CulturedDendritesEmbryonic DevelopmentGlycineMiceMice, KnockoutMotor NeuronsNeuronal PlasticityNeurotransmitter AgentsSynapsesGlycineNeurotransmitter Agentsdendritesgephyringlycine receptorshypoglossalmotoneuronsynaptic activity

Identifiers

PMID26740651
PMCPMC6601792
OpenAlexW2232443052

What OpenQuestion holds

Textmetadata
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.