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BDNF signaling and survival of striatal neurons

The striatum, a major component of the basal ganglia, performs multiple functions including control of movement, reward, and addiction. Dysfunction and death of striatal neurons are the main causes for the motor disorders associated with Huntington’s disease (HD). Brain-derived neurotrophic factor (...

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Detalles Bibliográficos
Autores principales: Baydyuk, Maryna, Xu, Baoji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4147651/
https://www.ncbi.nlm.nih.gov/pubmed/25221473
http://dx.doi.org/10.3389/fncel.2014.00254
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author Baydyuk, Maryna
Xu, Baoji
author_facet Baydyuk, Maryna
Xu, Baoji
author_sort Baydyuk, Maryna
collection PubMed
description The striatum, a major component of the basal ganglia, performs multiple functions including control of movement, reward, and addiction. Dysfunction and death of striatal neurons are the main causes for the motor disorders associated with Huntington’s disease (HD). Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, is among factors that promote survival and proper function of this neuronal population. Here, we review recent studies showing that BDNF determines the size of the striatum by supporting survival of the immature striatal neurons at their origin, promotes maturation of striatal neurons, and facilitates establishment of striatal connections during brain development. We also examine the role of BDNF in maintaining proper function of the striatum during adulthood, summarize the mechanisms that lead to a deficiency in BDNF signaling and subsequently striatal degeneration in HD, and highlight a potential role of BDNF as a therapeutic target for HD treatment.
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spelling pubmed-41476512014-09-12 BDNF signaling and survival of striatal neurons Baydyuk, Maryna Xu, Baoji Front Cell Neurosci Neuroscience The striatum, a major component of the basal ganglia, performs multiple functions including control of movement, reward, and addiction. Dysfunction and death of striatal neurons are the main causes for the motor disorders associated with Huntington’s disease (HD). Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, is among factors that promote survival and proper function of this neuronal population. Here, we review recent studies showing that BDNF determines the size of the striatum by supporting survival of the immature striatal neurons at their origin, promotes maturation of striatal neurons, and facilitates establishment of striatal connections during brain development. We also examine the role of BDNF in maintaining proper function of the striatum during adulthood, summarize the mechanisms that lead to a deficiency in BDNF signaling and subsequently striatal degeneration in HD, and highlight a potential role of BDNF as a therapeutic target for HD treatment. Frontiers Media S.A. 2014-08-28 /pmc/articles/PMC4147651/ /pubmed/25221473 http://dx.doi.org/10.3389/fncel.2014.00254 Text en Copyright © 2014 Baydyuk and Xu. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Baydyuk, Maryna
Xu, Baoji
BDNF signaling and survival of striatal neurons
title BDNF signaling and survival of striatal neurons
title_full BDNF signaling and survival of striatal neurons
title_fullStr BDNF signaling and survival of striatal neurons
title_full_unstemmed BDNF signaling and survival of striatal neurons
title_short BDNF signaling and survival of striatal neurons
title_sort bdnf signaling and survival of striatal neurons
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4147651/
https://www.ncbi.nlm.nih.gov/pubmed/25221473
http://dx.doi.org/10.3389/fncel.2014.00254
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