BDNF Regulates Rab11-Mediated Recycling Endosome Dynamics to Induce Dendritic Branching
Author
dc.contributor.author
Lazo, Óscar M.
Author
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González, Andrés
es_CL
Author
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Ascaño, María
es_CL
Author
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Kuruvilla, Rejji
es_CL
Author
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Couve Correa, Andrés
es_CL
Author
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Bronfman, Francisca
es_CL
Admission date
dc.date.accessioned
2014-02-04T18:12:35Z
Available date
dc.date.available
2014-02-04T18:12:35Z
Publication date
dc.date.issued
2013
Cita de ítem
dc.identifier.citation
J. Neurosci., April 3, 2013 • 33(14):6112– 6122
en_US
Identifier
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DOI:10.1523/JNEUROSCI.4630-12.2013
Identifier
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https://repositorio.uchile.cl/handle/2250/129248
General note
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Artículo de publicación ISI
en_US
Abstract
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Dendritic arborization of neurons is regulated by brain-derived neurotrophic factor (BDNF) together with its receptor, TrkB. Endocytosis
is required for dendritic branching and regulates TrkB signaling, but how postendocytic trafficking determines the neuronal response to
BDNF is not well understood. The monomeric GTPase Rab11 regulates the dynamics of recycling endosomes and local delivery of
receptors to specific dendritic compartments. We investigated whether Rab11-dependent trafficking of TrkB in dendrites regulates
BDNF-induced dendritic branching in rat hippocampal neurons. We report that TrkB in dendrites is a cargo for Rab11 endosomes and
that both Rab11 and its effector, MyoVb, are required for BDNF/TrkB-induced dendritic branching. In addition, BDNF induces the
accumulation of Rab11-positive endosomes and GTP-bound Rab11 in dendrites and the expression of a constitutively active mutant of
Rab11 is sufficient to increase dendritic branching by increasing TrkB localization in dendrites and enhancing sensitization to endogenous
BDNF. We propose that Rab11-dependent dendritic recycling provides a mechanism to retain TrkB in dendrites and to increase
local signaling to regulate arborization.