Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in fmr1 knock-out mice

Benjamin C. Reiner, Anna Dunaevsky

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Article numbere0126572
JournalPloS one
Volume10
Issue number5
DOIs
StatePublished - May 7 2015

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Dendritic Spines
Knockout Mice
Cluster Analysis
learning
Stabilization
Learning
Fragile X Syndrome
mice
Combustion knock
Forelimb
forelimbs
Intellectual Disability
Plasticity
animal models
image analysis
Imaging techniques

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General

Cite this

Deficit in motor training-induced clustering, but not stabilization, of new dendritic spines in fmr1 knock-out mice. / Reiner, Benjamin C.; Dunaevsky, Anna.

In: PloS one, Vol. 10, No. 5, e0126572, 07.05.2015.

Research output: Contribution to journalArticle

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