ArticleScientific reports2017
Investigation of hippocampal synaptic transmission and plasticity in mice deficient in the actin-binding protein Drebrin.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Exploring the AAK1 Phospho-signaling Landscape Through Phospho-centric Co-regulation Network.Cell biochemistry and biophysics · 2026Article
- Article
- Phosphoprofile reorganization of the actin binding protein Drebrin during long term depression.Frontiers in molecular neuroscience · 2025Article
- Exploring molecular signatures related to the mechanism of aging in different brain regions by integrated bioinformatics.Frontiers in molecular neuroscience · 2023Article
- Peroxisomal Proliferator-Activated ReceptorFrontiers in pharmacology · 2022Article
- The actin binding protein drebrin helps to protect against the development of seizure-like events in the entorhinal cortex.Scientific reports · 2021Article
- Drebrin controls scar formation and astrocyte reactivity upon traumatic brain injury by regulating membrane trafficking.Nature communications · 2021Article
- PTEN in Autism and Neurodevelopmental Disorders.Cold Spring Harbor perspectives in medicine · 2019Review
- ATM phosphorylation of the actin-binding protein drebrin controls oxidation stress-resistance in mammalian neurons and C. elegans.Nature communications · 2019Article
- Drebrin Isoforms Critically Regulate NMDAR- and mGluR-Dependent LTD Induction.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dynamic regulation of the actin cytoskeleton plays a key role in controlling the structure and function of synapses. It is vital for activity-dependent modulation of synaptic transmission and long-term changes in synaptic morphology associated with memory consolidation. Several regulators of actin dynamics at the synapse have been identified, of which a salient one is the postsynaptic actin stabilising protein Drebrin (DBN). It has been suggested that DBN modulates neurotransmission and changes in dendritic spine morphology associated with synaptic plasticity. Given that a decrease in DBN levels is correlated with cognitive deficits associated with ageing and dementia, it was hypothesised that DBN protein abundance instructs the integrity and function of synapses. We created a novel DBN deficient mouse line. Analysis of gross brain and neuronal morphology revealed no phenotype in the absence of DBN. Electrophysiological recordings in acute hippocampal slices and primary hippocampal neuronal cultures showed that basal synaptic transmission, and both long-term and homeostatic synaptic plasticity were unchanged, suggesting that loss of DBN is not sufficient in inducing synapse dysfunction. We propose that the overall lack of changes in synaptic function and plasticity in DBN deficient mice may indicate robust compensatory mechanisms that safeguard cytoskeleton dynamics at the synapse.
Identifiers
What OpenQuestion holds
Registered trials
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.