@article{ref1,
title="Motor-skill learning is dependent on astrocytic activity",
journal="Neural plasticity",
year="2015",
author="Padmashri, Ragunathan and Suresh, Anand and Boska, Michael D. and Dunaevsky, Anna",
volume="2015",
number="",
pages="e938023-e938023",
abstract="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 Ca(2+) 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 Ca(2+) signaling during a reaching task is necessary for motor-skill learning.<p /> <p>Language: en</p>",
language="en",
issn="2090-5904",
doi="10.1155/2015/938023",
url="http://dx.doi.org/10.1155/2015/938023"
}