Evidence map›Paper›PMID 31597723›Full record

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

Tiam1 is Critical for Glutamatergic Synapse Structure and Function in the Hippocampus.

Sadhna Rao, Yuni Kay, Bruce E Herring

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  8. Presynaptic Rac1 in the hippocampus selectively regulates working memory.bioRxiv : the preprint server for biology · 2024
    Article
  9. Article
  10. Protein 4.1N Plays a Cell Type-Specific Role in Hippocampal Glutamatergic Synapse Regulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  11. Synaptic memory and CaMKII.Physiological reviews · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Autism Spectrum Disorder/Intellectual Disability-Associated Mutations in Trio Disrupt Neuroligin 1-Mediated Synaptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Sadhna RaoDepartment of Biological Sciences, and.
Yuni KayDepartment of Biological Sciences, and.
Bruce E HerringDepartment of Biological Sciences, and bherring@usc.edu.
University of Southern California · US

Funding

Uncovering the Role of TRIO in Synaptic Function and Autism Spectrum DisorderR01NS112480 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HERRING, BRUCE · 2019 to 2023
$1.8M
Kalirin-7's role in synaptic transmission, plasticity and learning and memoryR00MH103398 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HERRING, BRUCE · 2016 to 2018
$730k
Kalirin-7's role in synaptic transmission, plasticity and learning and memoryK99MH103398 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HERRING, BRUCE · 2014 to 2015
$176k
NIMH NIH HHS K99 MH103398NIMH NIH HHS R00 MH103398NINDS NIH HHS R01 NS112480
6 · The paper itself

Abstract

Mounting evidence suggests numerous glutamatergic synapse subtypes exist in the brain, and that these subtypes are likely defined by unique molecular regulatory mechanisms. Recent work has identified substantial divergence of molecular composition between commonly studied Schaffer collateral synapses and perforant path-dentate gyrus (DG) synapses of the hippocampus. However, little is known about the molecular mechanisms that may confer unique properties to perforant path-DG synapses. Here we investigate whether the RhoGEF (Rho guanine-nucleotide exchange factor) protein Tiam1 plays a unique role in the regulation of glutamatergic synapses in dentate granule neurons using a combination of molecular, electrophysiological, and imaging approaches in rat entorhino-hippocampal slices of both sexes. We find that inhibition of Tiam1 function in dentate granule neurons reduces synaptic AMPA receptor function and causes dendritic spines to adopt an elongated filopodia-like morphology. We also find that Tiam1's support of perforant path-DG synapse function is dependent on its GEF domain and identify a potential role for the auto-inhibitory PH domain of Tiam1 in regulating Tiam1 function at these synapses. In marked contrast, reduced Tiam1 expression in CA1 pyramidal neurons produced no effect on glutamatergic synapse development. Together, these data identify a critical role for Tiam1 in the hippocampus and reveal a unique Tiam1-mediated molecular program of glutamatergic synapse regulation in dentate granule neurons.

Indexed as

AnimalsAnimals, NewbornDentate GyrusFemaleGlutamic AcidHippocampusMaleOrgan Culture TechniquesRatsRats, Sprague-DawleySynapsesT-Lymphoma Invasion and Metastasis-inducing Protein 1Glutamic AcidTiam1 protein, ratT-Lymphoma Invasion and Metastasis-inducing Protein 1dentate gyrushippocampusmaturationRhoGEFsynapseTiam1

Identifiers

PMID31597723
PMCPMC6867819
OpenAlexW2979800294

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.