Evidence map›Paper›PMID 27217145›Full record

ArticleMolecular psychiatry2017

Conditional ablation of neuroligin-1 in CA1 pyramidal neurons blocks LTP by a cell-autonomous NMDA receptor-independent mechanism.

M Jiang, J Polepalli, L Y Chen, B Zhang, T C Südhof, R C Malenka

Open access · greenAbstract read
In one paragraph

Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. 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
  3. Article
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  5. Review
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  7. Review
  8. Review
  9. Article
  10. Article
  11. Neurexin-β Mediates the Synaptogenic Activity of Amyloid Precursor Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Review
  13. Article
  14. Unique transsynaptic complexes enable long-term synaptic plasticity in a synapse-specific manner.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Article
  16. Review
  17. Transsynaptic cerebellin 4-neogenin 1 signaling mediates LTP in the mouse dentate gyrus.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Article
  19. Article
  20. MAGUKs are essential, but redundant, in long-term potentiation.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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.

M JiangDepartment of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
J PolepalliNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA.
L Y ChenDepartment of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
B ZhangDepartment of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
T C SüdhofDepartment of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
R C MalenkaNancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Stanford University · USHoward Hughes Medical Institute · US

Funding

Role of synaptotagmins and neurexin ligands in homeostatic synaptic plasticityP50MH086403 · NIMH · STANFORD UNIVERSITY · PI DEISSEROTH, KARL A. · 2009 to 2019
$18.4M
NIMH NIH HHS P50 MH086403
6 · The paper itself

Abstract

Neuroligins are postsynaptic cell-adhesion molecules implicated in autism and other neuropsychiatric disorders. Despite extensive work, the role of neuroligins in synapse function and plasticity, especially N-methyl-d-aspartate (NMDA) receptor (NMDAR)-dependent long-term potentiation (LTP), remains unclear. To establish which synaptic functions unequivocally require neuroligins, we analyzed single and triple conditional knockout (cKO) mice for all three major neuroligin isoforms (NL1-NL3). We inactivated neuroligins by stereotactic viral expression of Cre-recombinase in hippocampal CA1 region pyramidal neurons at postnatal day 0 (P0) or day 21 (P21) and measured synaptic function, synaptic plasticity and spine numbers in acute hippocampal slices 2-3 weeks later. Surprisingly, we find that ablation of neuroligins in newborn or juvenile mice only modestly impaired basal synaptic function in hippocampus and caused no alteration in postsynaptic spine numbers. However, triple cKO of NL1-NL3 or single cKO of NL1 impaired NMDAR-mediated excitatory postsynaptic currents and abolished NMDAR-dependent LTP. Strikingly, the NL1 cKO also abolished LTP elicited by activation of L-type Ca

Indexed as

AnimalsCA1 Region, HippocampalCell Adhesion Molecules, NeuronalElectric StimulationExcitatory Postsynaptic PotentialsHippocampusLong-Term PotentiationMaleMembrane ProteinsMiceMice, KnockoutNerve Tissue ProteinsNeuronal PlasticityPatch-Clamp TechniquesPyramidal CellsReceptors, N-Methyl-D-AspartateCell Adhesion Molecules, NeuronalMembrane ProteinsNerve Tissue Proteinsneuroligin 1Receptors, N-Methyl-D-Aspartate

Identifiers

PMID27217145
PMCPMC5122464
OpenAlexW2405294767

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.