Exploring new roles for actin upon LTP induction in dendritic spines

Mayte Bonilla-Quintana,Florentin Wörgötter

doi:10.1038/s41598-021-86367-z

Mayte Bonilla-Quintana, Florentin Wörgötter

Open Access

https://doi.org/10.1038/s41598-021-86367-z

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Abstract

Dendritic spines, small protrusions of the dendrites, enlarge upon LTP induction, linking morphological and functional properties. Although the role of actin in spine enlargement has been well studied, little is known about its relationship with mechanical membrane properties, such as membrane tension, which is involved in many cell processes, like exocytosis. Here, we use a 3D model of the dendritic spine to investigate how polymerization of actin filaments can effectively elevate the membrane tension to trigger exocytosis in a domain close to the tip of the spine. Moreover, we show that the same pool of actin promotes full membrane fusion after exocytosis and spine stabilization.

Highlights

IntroductionSmall protrusions of the dendrites, enlarge upon LTP induction, linking morphological and functional properties
Dendritic spines, small protrusions of the dendrites, enlarge upon LTP induction, linking morphological and functional properties
We find that a single F-actin polymerization focus located near the postsynaptic density (PSD) increases membrane tension most efficiently and aids membrane fusion and spine stabilization, suggesting that these events co-localize and result from a continuous reorganization of actin in this focus

Summary

Introduction

Small protrusions of the dendrites, enlarge upon LTP induction, linking morphological and functional properties. Such an increase in AMPA-receptor-mediated current is due to an increment of AMPARs at the synapse by exocytosis or lateral m ovement[2,3] It enhances the signal transmission between two neurons, thereby strengthening their synapse in a process called long-term potentiation (LTP, see Fig. 1 for a schematic description). These activity-dependent structural modifications of dendritic spines are thought to be the cellular basis for learning and memory[1]. According to Honkura et al.[8], this pool of actin is different to the dynamic and static pool because it requires calmodulin activation and has a treadmilling velocity of 2–15 min It is necessary for long-lasting spine enlargement.

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