Evidence map›Paper›PMID 26637799›Full record

ArticleNeuron2015

Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse.

Mónica S Montesinos, Wei Dong, Kevin Goff, Brati Das, Debbie Guerrero-Given, Robert Schmalzigaug, Richard T Premont, Rachel Satterfield, Naomi Kamasawa, Samuel M Young

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Presynaptic CabioRxiv : the preprint server for biology · 2026
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  4. Presynaptic αNeuron · 2025
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  18. Presynaptic NMDARs and astrocytes ally to control circuit-specific information flow.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  19. Article
  20. CaNeuron · 2019
    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

10 authors at 2 institutions in 1 country.

Mónica S MontesinosResearch Group Molecular Mechanisms of Synaptic Function, Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA.
Wei DongResearch Group Molecular Mechanisms of Synaptic Function, Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA.
Kevin GoffResearch Group Molecular Mechanisms of Synaptic Function, Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA.
Brati DasResearch Group Molecular Mechanisms of Synaptic Function, Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA; Integrative Program in Biology and Neuroscience, Florida Atlantic University, Jupiter, FL 33458, USA.
Debbie Guerrero-GivenMax Planck Florida Institute for Neuroscience Electron Microscopy Facility, Jupiter, FL 33458, USA.
Robert SchmalzigaugDivison of Gastroenterology, Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Richard T PremontDivison of Gastroenterology, Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Rachel SatterfieldResearch Group Molecular Mechanisms of Synaptic Function, Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA.
Naomi KamasawaMax Planck Florida Institute for Neuroscience Electron Microscopy Facility, Jupiter, FL 33458, USA.
Samuel M YoungResearch Group Molecular Mechanisms of Synaptic Function, Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458, USA. Electronic address: sam.young@mpfi.org.
Max Planck Florida Institute for Neuroscience · USDuke Medical Center · US

Funding

Regulation of Synaptic Vesicle Dynamics in the Auditory SystemR01DC014093 · NIDCD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI YOUNG, SAMUEL MATTHEW · 2015 to 2024
$3.7M
PTSD-like phenotype of mice lacking GIT2R21MH090556 · NIMH · DUKE UNIVERSITY · PI PREMONT, RICHARD T · 2010 to 2011
$421k
NIDCD NIH HHS R01 DC014093NIDCD NIH HHS R01 DC014093-01NIMH NIH HHS R21 MH090556
6 · The paper itself

Abstract

A cytomatrix of proteins at the presynaptic active zone (CAZ) controls the strength and speed of neurotransmitter release at synapses in response to action potentials. However, the functional role of many CAZ proteins and their respective isoforms remains unresolved. Here, we demonstrate that presynaptic deletion of the two G protein-coupled receptor kinase-interacting proteins (GITs), GIT1 and GIT2, at the mouse calyx of Held leads to a large increase in AP-evoked release with no change in the readily releasable pool size. Selective presynaptic GIT1 ablation identified a GIT1-specific role in regulating release probability that was largely responsible for increased synaptic strength. Increased synaptic strength was not due to changes in voltage-gated calcium channel currents or activation kinetics. Quantitative electron microscopy revealed unaltered ultrastructural parameters. Thus, our data uncover distinct roles for GIT1 and GIT2 in regulating neurotransmitter release strength, with GIT1 as a specific regulator of presynaptic release probability.

Indexed as

AnimalsAnimals, NewbornBiophysicsBrainCell Cycle ProteinsElectric StimulationExcitatory Postsynaptic PotentialsGreen Fluorescent ProteinsGTPase-Activating ProteinsIntercellular Signaling Peptides and ProteinsIn Vitro TechniquesMiceMice, KnockoutMicroscopy, Electron, TransmissionPatch-Clamp TechniquesPhosphoproteinsCell Cycle Proteinsenhanced green fluorescent proteinGit1 protein, mouseGit2 protein, mouseGreen Fluorescent ProteinsGTPase-Activating ProteinsIntercellular Signaling Peptides and ProteinsPhosphoproteinsVesicular Glutamate Transport Protein 2

Identifiers

PMID26637799
PMCPMC4672385
OpenAlexW2188027488

What OpenQuestion holds

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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.