Evidence map›Paper›PMID 21555073›Full record

ArticleNeuron2011

Neurexin-neuroligin transsynaptic interaction mediates learning-related synaptic remodeling and long-term facilitation in aplysia.

Yun-Beom Choi, Hsiu-Ling Li, Stefan R Kassabov, Iksung Jin, Sathyanarayanan V Puthanveettil, Kevin A Karl, Yang Lu, Joung-Hun Kim, Craig H Bailey, Eric R Kandel

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.8field-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

46 citing papers in PubMed, 93 citations in OpenAlex.

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  8. Anterograde and retrograde signaling by anProceedings of the National Academy of Sciences of the United States of America · 2018
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  12. Cell-Specific PKM Isoforms Contribute to the Maintenance of Different Forms of Persistent Long-Term Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
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  13. Article
  14. Inability to activate Rac1-dependent forgetting contributes to behavioral inflexibility in mutants of multiple autism-risk genes.Proceedings of the National Academy of Sciences of the United States of America · 2016
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  15. Synapse Formation in Monosynaptic Sensory-Motor Connections Is Regulated by Presynaptic Rho GTPase Cdc42.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
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  16. Article
  17. A Serotonin Circuit Acts as an Environmental Sensor to Mediate Midline Axon Crossing through EphrinB2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  18. Article
  19. Article
  20. Structural Components of Synaptic Plasticity and Memory Consolidation.Cold Spring Harbor perspectives in biology · 2015
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Yun-Beom ChoiDepartment of Neurology, College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, New York, NY 10032, USA.
Hsiu-Ling Li
Stefan R Kassabov
Iksung Jin
Sathyanarayanan V Puthanveettil
Kevin A Karl
Yang Lu
Joung-Hun Kim
Craig H Bailey
Eric R Kandel
Columbia University · USNew York State Psychiatric InstitutePohang University of Science and Technology · KR

Funding

Neurexin-Neuroligin Trans-synaptic Interaction: Learning-related Synaptic GrowthK08NS053415 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CHOI, YUN-BEOM · 2007 to 2011
$844k
Howard Hughes Medical InstituteNINDS NIH HHS K08 NS053415NINDS NIH HHS NS053415
6 · The paper itself

Abstract

Neurexin and neuroligin, which undergo heterophilic interactions with each other at the synapse, are mutated in some patients with autism spectrum disorder, a set of disorders characterized by deficits in social and emotional learning. We have explored the role of neurexin and neuroligin at sensory-to-motor neuron synapses of the gill-withdrawal reflex in Aplysia, which undergoes sensitization, a simple form of learned fear. We find that depleting neurexin in the presynaptic sensory neuron or neuroligin in the postsynaptic motor neuron abolishes both long-term facilitation and the associated presynaptic growth induced by repeated pulses of serotonin. Moreover, introduction into the motor neuron of the R451C mutation of neuroligin-3 linked to autism spectrum disorder blocks both intermediate-term and long-term facilitation. Our results suggest that activity-dependent regulation of the neurexin-neuroligin interaction may govern transsynaptic signaling required for the storage of long-term memory, including emotional memory that may be impaired in autism spectrum disorder.

Indexed as

Analysis of VarianceAnimalsAplysiaArginineCell Adhesion Molecules, NeuronalCells, CulturedCentral Nervous SystemCloning, MolecularCysteineExcitatory Postsynaptic PotentialsGene Expression RegulationGreen Fluorescent ProteinsHumansLong-Term PotentiationMembrane ProteinsMicroinjectionsArginineCell Adhesion Molecules, NeuronalCysteineGreen Fluorescent ProteinsMembrane ProteinsNerve Tissue Proteinsneuroligin 3Nrxn1 protein, ratOligodeoxyribonucleotides, AntisenseReceptors, Cell SurfaceSerotonin

Identifiers

PMID21555073
PMCPMC3136118
OpenAlexW2152997919

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.