Neuron December 2015 PMID 26637799

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

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Mentions

Peak: 1 in Jan 2016

across 3 sources since Jan 2016

Extended reach

2,382

potential audience

Total likes

Video views

1,094

Mentions per month

Jan 2016 – Oct 2019

Where it's discussed

Blogs4 articles
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YouTube1 videos

AI synopsis

What people are saying

Discussions highlight the importance of GIT1's role in controlling neurotransmitter release, with posts describing the research as a 'breakthrough' and questioning its potential in neurological therapies. The tone suggests a blend of curiosity and recognition of the study's relevance, reflecting moderate to high engagement and perceived impact.

AgreementModerate agreement

Many discussions acknowledge the significance of the findings, with some emphasizing the role of GIT1 and GIT2 in synaptic regulation.

InterestModerate interest

Participants show moderate interest, often asking for further details or expressing curiosity about the implications of the research.

EngagementHigh engagement

Several posts delve into the mechanisms and potential applications, indicating deep engagement.

ImpactModerate impact

The consensus recognizes that the research advances understanding of synaptic processes, although some see it as foundational rather than immediately transformative.

Abstract in brief

The study shows that deleting GIT1 and GIT2 proteins in the presynaptic part of mammalian synapses increases neurotransmitter release without changing the size of the readily releasable pool, suggesting these proteins normally suppress release strength.
Specifically, removing GIT1 alone affects the release probability, highlighting its unique role in controlling how likely neurotransmitters are released during nerve signals, without altering calcium channel function or synapse structure.
Overall, GIT1 and GIT2 have distinct functions in regulating synaptic strength, with GIT1 acting as a key regulator of release probability, which impacts how strongly synapses respond to nerve impulses.]

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All mentions

GIT protein deletion results in increased synaptic strength at a mammalian central synapse

AJE Video Bytes · Jan 12, 2016 783 views

Impact of GIT Protein Deletion on Synaptic Strength in Mammalian Neurons

Montesinos et al. show that presynaptic deletion of GIT proteins increases neurotransmitter release at mammalian synapses, highlighting GIT1 and GIT2’s roles in suppressing synaptic strength without affecting synapse…

MPFNeuro · Apr 19, 2016 311 views

Rosaura Brisuela @roswitta.bsky.social

@Roswitamind · X

Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse:https://t.co/wfdaSlTSe0 https://t.co/1xCOgbG2Hu

Oct 1, 2019 · 1 like · 1,289 followers View post →