Investigation of hippocampal synaptic transmission and plasticity in mice deficient in the actin-binding protein Drebrin

Tools

Willmes, Claudia G. and Mack, Till G. A. and Ledderose, Julia and Schmitz, Dietmar and Wozny, Christian and Eickholt, Britta J. (2017) Investigation of hippocampal synaptic transmission and plasticity in mice deficient in the actin-binding protein Drebrin. Scientific Reports, 7. 42652. ISSN 2045-2322 (https://doi.org/10.1038/srep42652)

[thumbnail of Willmes-etal-SR-2017-Investigation-of-hippocampal-synaptic-transmission]
Preview
 Text. Filename: Willmes_etal_SR_2017_Investigation_of_hippocampal_synaptic_transmission.pdf
Final Published Version
License: Creative Commons Attribution 4.0 logo
Download (1MB)| Preview

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.

ORCID iDs

Willmes, Claudia G., Mack, Till G. A., Ledderose, Julia, Schmitz, Dietmar, Wozny, Christian ORCID logoORCID: https://orcid.org/0000-0003-4220-2033 and Eickholt, Britta J.;
CORE (COnnecting REpositories)