Evidence map›Paper›PMID 30871858›Full record

ArticleNeuron2019

Neuroligin-1 Signaling Controls LTP and NMDA Receptors by Distinct Molecular Pathways.

Xiaoting Wu, Wade K Morishita, Ashley M Riley, William D Hale, Thomas C Südhof, Robert C Malenka

Open access · greenAbstract read
In one paragraph

Article in Neuron, 2019. 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
7.0field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 90 citations in OpenAlex.

  1. Therapeutic Administration ofInternational journal of molecular sciences · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Neuroligin-2-Dependent Adhesion Defines a Molecular Checkpoint for Inhibitory Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. MDGAs perform activity-dependent synapse type-specific suppression via distinct extracellular mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Cell Adhesion Molecule Signaling at the Synapse: Beyond the Scaffold.Cold Spring Harbor perspectives in biology · 2024
    Review
  13. Article
  14. Article
  15. Altered plasma membrane abundance of the sulfatide-binding protein NF155 links glycosphingolipid imbalances to demyelination.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Review
  17. Article
  18. Engineered adhesion molecules drive synapse organization.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Xiaoting WuNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Wade K MorishitaNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ashley M RileyNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
William D HaleDepartment of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Thomas C SüdhofDepartment of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: tcs1@stanford.edu.
Robert C MalenkaNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: malenka@stanford.edu.
Howard Hughes Medical Institute · USStanford University · US

Funding

Role of synaptotagmins and neurexin ligands in homeostatic synaptic plasticityP50MH086403 · NIMH · STANFORD UNIVERSITY · PI DEISSEROTH, KARL A. · 2009 to 2019
$18.4M
Induced neuronal cells: A novel tool to study neuropsychiatric diseasesR01MH092931 · NIMH · STANFORD UNIVERSITY · PI Thomas C. Sudhof, Marius Wernig · 2010 to 2026
$9.7M
FUNCTION OF NEUREXINSR37MH052804 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI SUDHOF, THOMAS C. · 2000 to 2019
$9.3M
NIMH NIH HHS P50 MH086403NIMH NIH HHS R01 MH092931NIMH NIH HHS R37 MH052804
6 · The paper itself

Abstract

Neuroligins, postsynaptic cell adhesion molecules that are linked to neuropsychiatric disorders, are extensively studied, but fundamental questions about their functions remain. Using in vivo replacement strategies in quadruple conditional knockout mice of all neuroligins to avoid heterodimerization artifacts, we show, in hippocampal CA1 pyramidal neurons, that neuroligin-1 performs two key functions in excitatory synapses by distinct molecular mechanisms. N-methyl-D-aspartate (NMDA) receptor-dependent LTP requires trans-synaptic binding of postsynaptic neuroligin-1 to presynaptic β-neurexins but not the cytoplasmic sequences of neuroligins. In contrast, postsynaptic NMDA receptor (NMDAR)-mediated responses involve a neurexin-independent mechanism that requires the neuroligin-1 cytoplasmic sequences. Strikingly, deletion of neuroligins blocked the spine expansion associated with LTP, as monitored by two-photon imaging; this block involved a mechanism identical to that of the role of neuroligin-1 in NMDAR-dependent LTP. Our data suggest that neuroligin-1 performs two mechanistically distinct signaling functions and that neurolign-1-mediated trans-synaptic cell adhesion signaling critically regulates LTP.

Indexed as

AnimalsCA1 Region, HippocampalCell AdhesionCell Adhesion Molecules, NeuronalLong-Term PotentiationMembrane ProteinsMiceMice, KnockoutNerve Tissue ProteinsPyramidal CellsReceptors, N-Methyl-D-AspartateSynapsesCell Adhesion Molecules, NeuronalMembrane ProteinsNerve Tissue Proteinsneurexin Ibetaneurexin IIneurexin IIIbetaneuroligin 1neuroligin 2neuroligin 3Nlgn4 protein, mouseReceptors, N-Methyl-D-Aspartatecell adhesionhippocampuslong-term potentiationLTPneuroliginNMDA receptorplasticitysynapsetrans-synaptic

Identifiers

PMID30871858
PMCPMC6509009
OpenAlexW2922324150

What OpenQuestion holds

Textmetadata
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.