Evidence map›Paper›PMID 31578233›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Modeling a Neurexin-3α Human Mutation in Mouse Neurons Identifies a Novel Role in the Regulation of Transsynaptic Signaling and Neurotransmitter Release at Excitatory Synapses.

Susana Restrepo, Nora J Langer, Kylan A Nelson, Jason Aoto

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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  10. Kirrel3-Mediated Synapse Formation Is Attenuated by Disease-Associated Missense Variants.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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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

4 authors at 1 institution in 1 country.

Susana RestrepoDepartment of Pharmacology, University of Colorado Denver School of Medicine, Aurora, Colorado 80045.ORCID 0000-0003-4466-5920
Nora J LangerDepartment of Pharmacology, University of Colorado Denver School of Medicine, Aurora, Colorado 80045.
Kylan A NelsonDepartment of Pharmacology, University of Colorado Denver School of Medicine, Aurora, Colorado 80045.
Jason AotoDepartment of Pharmacology, University of Colorado Denver School of Medicine, Aurora, Colorado 80045 jason.aoto@ucdenver.edu.ORCID 0000-0003-0568-634X
University of Colorado Denver · US

Funding

PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM007635 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 1985 to 2023
$6.1M
Functional and mechanistic interrogation of alpha neurexin extracellular domainsR01MH116901 · NIMH · UNIVERSITY OF COLORADO DENVER · PI AOTO, JASON · 2018 to 2022
$1.9M
Synaptic Dissection of Cell Adhesion Molecule Function within Subicular CircuitsR00MH103531 · NIMH · UNIVERSITY OF COLORADO DENVER · PI AOTO, JASON · 2016 to 2018
$746k
NIGMS NIH HHS T32 GM007635NIMH NIH HHS R00 MH103531NIMH NIH HHS R01 MH116901
6 · The paper itself

Abstract

Presynaptic α-neurexins are highly expressed and more frequently linked to neuropsychiatric and neurodevelopmental disorders than β-neurexins. However, how extracellular sequences specific to α-neurexins enable synaptic transmission is poorly understood. We identified a mutation in an extracellular region of neurexin-3α (A687T), located in a region conserved among α-neurexins and throughout vertebrate evolution, in a patient diagnosed with profound intellectual disability and epilepsy. We systematically interrogated this mutation using a knockdown-replacement approach, and discovered that the A687T mutation enhanced presynaptic morphology and increased two critical presynaptic parameters: (1) presynaptic release probability, and (2) the size of the readily releasable pool exclusively at excitatory synapses in mixed sex primary mouse hippocampal cultures. Introduction of the mutation

Indexed as

AnimalsEpilepsyExcitatory Postsynaptic PotentialsFemaleGene Knockdown TechniquesHEK293 CellsHippocampusHumansIntellectual DisabilityMaleMice, Inbred C57BLMutation, MissenseNerve Tissue ProteinsNeuronsPrimary Cell CultureProtein TransportNerve Tissue Proteinsneurexin IIIalphahuman mutationneurexinpresynaptic releaseα neurexin

Identifiers

PMID31578233
PMCPMC6855690
OpenAlexW2978511027

What OpenQuestion holds

Textmetadata
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.