Evidence map›Paper›PMID 33355091›Full record

ArticleeLife2020

Specific Neuroligin3-αNeurexin1 signaling regulates GABAergic synaptic function in mouse hippocampus.

Motokazu Uchigashima, Kohtarou Konno, Emily Demchak, Amy Cheung, Takuya Watanabe, David G Keener, Manabu Abe, Timmy Le, Kenji Sakimura, Toshikuni Sasaoka and 4 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Alpha-neurexins in health and disease.Frontiers in molecular neuroscience · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Conserved autism-associated genes tune social feeding behavior inbioRxiv : the preprint server for biology · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

14 authors at 5 institutions in 2 countries.

Motokazu UchigashimaBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, United States.ORCID 0000-0002-0878-2233
Kohtarou KonnoDepartment of Anatomy, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Emily DemchakDepartment of Biochemistry and Molecular Biology and Institute for Personalized Medicine, Pennsylvania State University College of Medicine, Hershey, United States.
Amy CheungBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, United States.ORCID 0000-0002-4708-0293
Takuya WatanabeBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, United States.
David G KeenerBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, United States.
Manabu AbeDepartment of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Japan.
Timmy LeBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, United States.
Kenji SakimuraDepartment of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Japan.
Toshikuni SasaokaDepartment of Comparative and Experimental Medicine, Brain Research Institute, Niigata University, Niigata, Japan.
Takeshi UemuraDivision of Gene Research, Research Center for Supports to Advanced Science, Shinshu University, Nagano, Japan.
Yuka Imamura KawasawaDepartment of Biochemistry and Molecular Biology and Institute for Personalized Medicine, Pennsylvania State University College of Medicine, Hershey, United States.
Masahiko WatanabeDepartment of Anatomy, Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0001-5037-7138
Kensuke FutaiBrudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, United States.ORCID 0000-0002-3433-3407
University of Massachusetts Chan Medical School · USNiigata University · JPHokkaido University · JPPennsylvania State University · USShinshu University · JP

Funding

Medical Scientist Training at UMMS Administrative SupplementT32GM107000 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIEFE, CATARINA I. · 2013 to 2022
$4.9M
Functional analysis of Neuroligin-Neurexin interactions in synaptic transmissionR01NS085215 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FUTAI, KENSUKE · 2014 to 2018
$1.8M
The role of Neurexin in serotonin synaptic function and social behaviorF30MH122146 · NIMH · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CHEUNG, AMY · 2020 to 2022
$78k
NIGMS NIH HHS T32 GM107000NIMH NIH HHS F30 MH122146NINDS NIH HHS R01 NS085215
6 · The paper itself

Abstract

Synapse formation and regulation require signaling interactions between pre- and postsynaptic proteins, notably cell adhesion molecules (CAMs). It has been proposed that the functions of neuroligins (Nlgns), postsynaptic CAMs, rely on the formation of trans-synaptic complexes with neurexins (Nrxns), presynaptic CAMs. Nlgn3 is a unique Nlgn isoform that localizes at both excitatory and inhibitory synapses. However, Nlgn3 function mediated via Nrxn interactions is unknown. Here we demonstrate that Nlgn3 localizes at postsynaptic sites apposing vesicular glutamate transporter 3-expressing (VGT3+) inhibitory terminals and regulates VGT3+ inhibitory interneuron-mediated synaptic transmission in mouse organotypic slice cultures. Gene expression analysis of interneurons revealed that the αNrxn1+AS4 splice isoform is highly expressed in VGT3+ interneurons as compared with other interneurons. Most importantly, postsynaptic Nlgn3 requires presynaptic αNrxn1+AS4 expressed in VGT3+ interneurons to regulate inhibitory synaptic transmission. Our results indicate that specific Nlgn-Nrxn signaling generates distinct functional properties at synapses.

Indexed as

AnimalsCA1 Region, HippocampalCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalFemaleGABAergic NeuronsGene Knockdown TechniquesHippocampusMaleMembrane ProteinsMiceMice, Inbred C57BLNerve Tissue ProteinsNeural Cell Adhesion MoleculesSynapsesCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalMembrane ProteinsNerve Tissue ProteinsNeural Cell Adhesion Moleculesneuroligin 3Nrxn1 protein, mouseelectrophysiologyhippocampusinhibitory interneuronmouseneurosciencetrans-synaptic adhesion

Identifiers

PMID33355091
PMCPMC7758064
OpenAlexW3117436196

What OpenQuestion holds

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Registered trials

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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.