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Long-term depression and other synaptic plasticity in the cerebellum

Cerebellar long-term depression (LTD) is a type of synaptic plasticity and has been considered as a critical cellular mechanism for motor learning. LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to tr...

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Autor principal: HIRANO, Tomoo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japan Academy 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3722574/
https://www.ncbi.nlm.nih.gov/pubmed/23666089
http://dx.doi.org/10.2183/pjab.89.183
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author HIRANO, Tomoo
author_facet HIRANO, Tomoo
author_sort HIRANO, Tomoo
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description Cerebellar long-term depression (LTD) is a type of synaptic plasticity and has been considered as a critical cellular mechanism for motor learning. LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to transmitter glutamate. Molecular induction mechanism of LTD has been intensively studied using culture and slice preparations, which has revealed critical roles of Ca(2+), protein kinase C and endocytosis of AMPA-type glutamate receptors. Involvement of a large number of additional molecules has also been demonstrated, and their interactions relevant to LTD mechanisms have been studied. In vivo experiments including those on mutant mice, have reported good correlation of LTD and motor learning. However, motor learning could occur with impaired LTD. A possibility that cerebellar synaptic plasticity other than LTD compensates for the defective LTD has been proposed.
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spelling pubmed-37225742013-08-09 Long-term depression and other synaptic plasticity in the cerebellum HIRANO, Tomoo Proc Jpn Acad Ser B Phys Biol Sci Review Cerebellar long-term depression (LTD) is a type of synaptic plasticity and has been considered as a critical cellular mechanism for motor learning. LTD occurs at excitatory synapses between parallel fibers and a Purkinje cell in the cerebellar cortex, and is expressed as reduced responsiveness to transmitter glutamate. Molecular induction mechanism of LTD has been intensively studied using culture and slice preparations, which has revealed critical roles of Ca(2+), protein kinase C and endocytosis of AMPA-type glutamate receptors. Involvement of a large number of additional molecules has also been demonstrated, and their interactions relevant to LTD mechanisms have been studied. In vivo experiments including those on mutant mice, have reported good correlation of LTD and motor learning. However, motor learning could occur with impaired LTD. A possibility that cerebellar synaptic plasticity other than LTD compensates for the defective LTD has been proposed. The Japan Academy 2013-05-10 /pmc/articles/PMC3722574/ /pubmed/23666089 http://dx.doi.org/10.2183/pjab.89.183 Text en Copyright © 2013 The Japan Academy This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
HIRANO, Tomoo
Long-term depression and other synaptic plasticity in the cerebellum
title Long-term depression and other synaptic plasticity in the cerebellum
title_full Long-term depression and other synaptic plasticity in the cerebellum
title_fullStr Long-term depression and other synaptic plasticity in the cerebellum
title_full_unstemmed Long-term depression and other synaptic plasticity in the cerebellum
title_short Long-term depression and other synaptic plasticity in the cerebellum
title_sort long-term depression and other synaptic plasticity in the cerebellum
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3722574/
https://www.ncbi.nlm.nih.gov/pubmed/23666089
http://dx.doi.org/10.2183/pjab.89.183
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