Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.

Fragile X Syndrome is the most common inherited intellectual disability, and Fragile X Syndrome patients often exhibit motor and learning deficits. It was previously shown that the fmr1 knock-out mice, a common mouse model of Fragile X Syndrome, recapitulates this motor learning deficit and that the...

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Main Authors: Benjamin C Reiner, Anna Dunaevsky
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4423947?pdf=render
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spelling doaj-abed722dee1f483fb00aeb075def56ae2020-11-25T01:51:13ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01105e012657210.1371/journal.pone.0126572Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.Benjamin C ReinerAnna DunaevskyFragile X Syndrome is the most common inherited intellectual disability, and Fragile X Syndrome patients often exhibit motor and learning deficits. It was previously shown that the fmr1 knock-out mice, a common mouse model of Fragile X Syndrome, recapitulates this motor learning deficit and that the deficit is associated with altered plasticity of dendritic spines. Here, we investigated the motor learning-induced turnover, stabilization and clustering of dendritic spines in the fmr1 knock-out mouse using a single forelimb reaching task and in vivo multiphoton imaging. We report that fmr1 knock-out mice have deficits in motor learning-induced changes in dendritic spine turnover and new dendritic spine clustering, but not the motor learning-induced long-term stabilization of new dendritic spines. These results suggest that a failure to establish the proper synaptic connections in both number and location, but not the stabilization of the connections that are formed, contributes to the motor learning deficit seen in the fmr1 knock-out mouse.http://europepmc.org/articles/PMC4423947?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Benjamin C Reiner
Anna Dunaevsky
spellingShingle Benjamin C Reiner
Anna Dunaevsky
Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.
PLoS ONE
author_facet Benjamin C Reiner
Anna Dunaevsky
author_sort Benjamin C Reiner
title Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.
title_short Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.
title_full Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.
title_fullStr Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.
title_full_unstemmed Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in FMR1 knock-out mice.
title_sort deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in fmr1 knock-out mice.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2015-01-01
description Fragile X Syndrome is the most common inherited intellectual disability, and Fragile X Syndrome patients often exhibit motor and learning deficits. It was previously shown that the fmr1 knock-out mice, a common mouse model of Fragile X Syndrome, recapitulates this motor learning deficit and that the deficit is associated with altered plasticity of dendritic spines. Here, we investigated the motor learning-induced turnover, stabilization and clustering of dendritic spines in the fmr1 knock-out mouse using a single forelimb reaching task and in vivo multiphoton imaging. We report that fmr1 knock-out mice have deficits in motor learning-induced changes in dendritic spine turnover and new dendritic spine clustering, but not the motor learning-induced long-term stabilization of new dendritic spines. These results suggest that a failure to establish the proper synaptic connections in both number and location, but not the stabilization of the connections that are formed, contributes to the motor learning deficit seen in the fmr1 knock-out mouse.
url http://europepmc.org/articles/PMC4423947?pdf=render
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AT annadunaevsky deficitinmotortraininginducedclusteringbutnotstabilizationofnewdendriticspinesinfmr1knockoutmice
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