Chemical LTD, but not LTP, induces transient accumulation of gelsolin in dendritic spines

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Hlushchenko , I & Hotulainen , P 2019 , ' Chemical LTD, but not LTP, induces transient accumulation of gelsolin in dendritic spines ' , Biological Chemistry , vol. 400 , no. 9 , pp. 1129-1139 . https://doi.org/10.1515/hsz-2019-0110

Title: Chemical LTD, but not LTP, induces transient accumulation of gelsolin in dendritic spines
Author: Hlushchenko, Iryna; Hotulainen, Pirta
Contributor: University of Helsinki, Neuroscience Center
Date: 2019-09
Number of pages: 11
Belongs to series: Biological Chemistry
ISSN: 1431-6730
URI: http://hdl.handle.net/10138/317097
Abstract: Synaptic plasticity underlies central brain functions, such as learning. Ca2+ signaling is involved in both strengthening and weakening of synapses, but it is still unclear how one signal molecule can induce two opposite outcomes. By identifying molecules, which can distinguish between signaling leading to weakening or strengthening, we can improve our understanding of how synaptic plasticity is regulated. Here, we tested gelsolin's response to the induction of chemical long-term potentiation (cLTP) or long-term depression (cLTD) in cultured rat hippocampal neurons. We show that gelsolin relocates from the dendritic shaft to dendritic spines upon cLTD induction while it did not show any relocalization upon cLTP induction. Dendritic spines are small actin-rich protrusions on dendrites, where LTD/LTP-responsive excitatory synapses are located. We propose that the LTD-induced modest - but relatively long-lasting - elevation of Ca2+ concentration increases the affinity of gelsolin to F-actin. As F-actin is enriched in dendritic spines, it is probable that increased affinity to F-actin induces the relocalization of gelsolin.
Subject: actin cytoskeleton
neurons
synaptic plasticity
LONG-TERM DEPRESSION
AMPA RECEPTOR TRAFFICKING
ACTIN DYNAMICS
CALCIUM
CA2+
LOCALIZATION
POTENTIATION
ACTIVATION
MECHANISMS
PLATFORM
1182 Biochemistry, cell and molecular biology
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