Evidence map›Paper›PMID 29107521›Full record

ArticleNeuron2017

Molecular Dissection of Neuroligin 2 and Slitrk3 Reveals an Essential Framework for GABAergic Synapse Development.

Jun Li, Wenyan Han, Kenneth A Pelkey, Jingjing Duan, Xia Mao, Ya-Xian Wang, Michael T Craig, Lijin Dong, Ronald S Petralia, Chris J McBain and 1 more

Abstract read
In one paragraph

Article in Neuron, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
–field-weighted citation impact
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

55 citing papers in PubMed.

  1. Review
  2. Article
  3. Network Activity Shapes Inhibitory Synaptic Development in the Mouse Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Reversing anxiety by targeting a stress-responsive signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Cell Adhesion Molecule Signaling at the Synapse: Beyond the Scaffold.Cold Spring Harbor perspectives in biology · 2024
    Review
  13. Structural and functional reorganization of inhibitory synapses by activity-dependent cleavage of neuroligin-2.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. GABAFrontiers in cellular neuroscience · 2024
    Article
  16. Human mutations inFrontiers in molecular neuroscience · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Jun LiSynapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Wenyan HanSynapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Kenneth A PelkeyProgram in Developmental Neuroscience, Eunice Kennedy-Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Jingjing DuanSynapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Xia MaoSynapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Ya-Xian WangAdvanced Imaging Core, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.
Michael T CraigInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, Hatherly Laboratories, University of Exeter, Prince of Wales Road, Exeter EX4 4PS, UK.
Lijin DongGenetic Engineering Core, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Ronald S PetraliaAdvanced Imaging Core, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA.
Chris J McBainProgram in Developmental Neuroscience, Eunice Kennedy-Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Wei LuSynapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: luw4@mail.nih.gov.

Funding

Cellular And Synaptic Physiology Of Hippocampal InterneuronsZIAHD001205 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MCBAIN, CHRIS J. · 2009 to 2025
$45.8M
The regulation of synaptic transmission and neural circuit functionZIANS003136 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI LU, WEI · 2012 to 2025
$27.0M
NEI Genetic Engineering CoreZICEY000458 · NEI · NATIONAL EYE INSTITUTE · PI DONG, LIJIN · 2009 to 2025
$22.6M
Advanced Imaging CoreZICDC000081 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI WINKLER, DENNIS · 2012 to 2025
$17.4M
Intramural NIH HHS Z99 NS999999
6 · The paper itself

Abstract

In the brain, many types of interneurons make functionally diverse inhibitory synapses onto principal neurons. Although numerous molecules have been identified to function in inhibitory synapse development, it remains unknown whether there is a unifying mechanism for development of diverse inhibitory synapses. Here we report a general molecular mechanism underlying hippocampal inhibitory synapse development. In developing neurons, the establishment of GABAergic transmission depends on Neuroligin 2 (NL2), a synaptic cell adhesion molecule (CAM). During maturation, inhibitory synapse development requires both NL2 and Slitrk3 (ST3), another CAM. Importantly, NL2 and ST3 interact with nanomolar affinity through their extracellular domains to synergistically promote synapse development. Selective perturbation of the NL2-ST3 interaction impairs inhibitory synapse development with consequent disruptions in hippocampal network activity and increased seizure susceptibility. Our findings reveal how unique postsynaptic CAMs work in concert to control synaptogenesis and establish a general framework for GABAergic synapse development.

Indexed as

AnimalsCell Adhesion Molecules, NeuronalCells, CulturedGABAergic NeuronsHippocampusMembrane ProteinsMice, KnockoutNerve Tissue ProteinsNeural InhibitionNeurogenesisSeizuresSynapsesSynaptic TransmissionCell Adhesion Molecules, NeuronalMembrane ProteinsNerve Tissue Proteinsneuroligin 2Slitrk5 protein, mousecell adhesion moleculecollybistindevelopmentGABAGABAergic synapsegamma oscillationgephyrinNeuroligin 2seizureSlitrk3

Identifiers

PMID29107521
PMCPMC5957482

What OpenQuestion holds

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LicenceTDM
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.