Motor-Skill Learning Is Dependent on Astrocytic Activity

Motor-skill learning induces changes in synaptic structure and function in the primary motor cortex through the involvement of a long-term potentiation- (LTP-) like mechanism. Although there is evidence that calcium-dependent release of gliotransmitters by astrocytes plays an important role in synap...

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Main Authors: Ragunathan Padmashri, Anand Suresh, Michael D. Boska, Anna Dunaevsky
Format: Article
Language:English
Published: Hindawi Limited 2015-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2015/938023
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spelling doaj-986ac879892e422cbb47960e9d4bc2db2020-11-24T22:32:12ZengHindawi LimitedNeural Plasticity2090-59041687-54432015-01-01201510.1155/2015/938023938023Motor-Skill Learning Is Dependent on Astrocytic ActivityRagunathan Padmashri0Anand Suresh1Michael D. Boska2Anna Dunaevsky3Department of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, NE 68198, USADepartment of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, NE 68198, USADepartment of Radiology, University of Nebraska Medical Center, Omaha, NE 68198, USADepartment of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, NE 68198, USAMotor-skill learning induces changes in synaptic structure and function in the primary motor cortex through the involvement of a long-term potentiation- (LTP-) like mechanism. Although there is evidence that calcium-dependent release of gliotransmitters by astrocytes plays an important role in synaptic transmission and plasticity, the role of astrocytes in motor-skill learning is not known. To test the hypothesis that astrocytic activity is necessary for motor-skill learning, we perturbed astrocytic function using pharmacological and genetic approaches. We find that perturbation of astrocytes either by selectively attenuating IP3R2 mediated astrocyte Ca2+ signaling or using an astrocyte specific metabolic inhibitor fluorocitrate (FC) results in impaired motor-skill learning of a forelimb reaching-task in mice. Moreover, the learning impairment caused by blocking astrocytic activity using FC was rescued by administration of the gliotransmitter D-serine. The learning impairments are likely caused by impaired LTP as FC blocked LTP in slices and prevented motor-skill training-induced increases in synaptic AMPA-type glutamate receptor in vivo. These results support the conclusion that normal astrocytic Ca2+ signaling during a reaching task is necessary for motor-skill learning.http://dx.doi.org/10.1155/2015/938023
collection DOAJ
language English
format Article
sources DOAJ
author Ragunathan Padmashri
Anand Suresh
Michael D. Boska
Anna Dunaevsky
spellingShingle Ragunathan Padmashri
Anand Suresh
Michael D. Boska
Anna Dunaevsky
Motor-Skill Learning Is Dependent on Astrocytic Activity
Neural Plasticity
author_facet Ragunathan Padmashri
Anand Suresh
Michael D. Boska
Anna Dunaevsky
author_sort Ragunathan Padmashri
title Motor-Skill Learning Is Dependent on Astrocytic Activity
title_short Motor-Skill Learning Is Dependent on Astrocytic Activity
title_full Motor-Skill Learning Is Dependent on Astrocytic Activity
title_fullStr Motor-Skill Learning Is Dependent on Astrocytic Activity
title_full_unstemmed Motor-Skill Learning Is Dependent on Astrocytic Activity
title_sort motor-skill learning is dependent on astrocytic activity
publisher Hindawi Limited
series Neural Plasticity
issn 2090-5904
1687-5443
publishDate 2015-01-01
description Motor-skill learning induces changes in synaptic structure and function in the primary motor cortex through the involvement of a long-term potentiation- (LTP-) like mechanism. Although there is evidence that calcium-dependent release of gliotransmitters by astrocytes plays an important role in synaptic transmission and plasticity, the role of astrocytes in motor-skill learning is not known. To test the hypothesis that astrocytic activity is necessary for motor-skill learning, we perturbed astrocytic function using pharmacological and genetic approaches. We find that perturbation of astrocytes either by selectively attenuating IP3R2 mediated astrocyte Ca2+ signaling or using an astrocyte specific metabolic inhibitor fluorocitrate (FC) results in impaired motor-skill learning of a forelimb reaching-task in mice. Moreover, the learning impairment caused by blocking astrocytic activity using FC was rescued by administration of the gliotransmitter D-serine. The learning impairments are likely caused by impaired LTP as FC blocked LTP in slices and prevented motor-skill training-induced increases in synaptic AMPA-type glutamate receptor in vivo. These results support the conclusion that normal astrocytic Ca2+ signaling during a reaching task is necessary for motor-skill learning.
url http://dx.doi.org/10.1155/2015/938023
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AT michaeldboska motorskilllearningisdependentonastrocyticactivity
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