The Rab11-regulated endocytic pathway and BDNF/TrkB signaling: Roles in plasticity changes and neurodegenerative diseases

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dc.contributor.authorMoya-Alvarado, Guillermo
dc.contributor.authorGuerra, Miguel V.
dc.contributor.authorTiburcio, Reynaldo
dc.contributor.authorBravo, Evelyn
dc.contributor.authorBronfman, Francisca C.
dc.date.accessioned2025-01-20T21:04:21Z
dc.date.available2025-01-20T21:04:21Z
dc.date.issued2022
dc.description.abstractNeurons are highly polarized cells that rely on the intracellular transport of organelles. This process is regulated by molecular motors such as dynein and kinesins and the Rab family of monomeric GTPases that together help move cargo along microtubules in dendrites, somas, and axons. Rab5-Rab11 GTPases regulate receptor trafficking along early-recycling endosomes, which is a process that determines the intracellular signaling output of different signaling pathways, including those triggered by BDNF binding to its tyrosine kinase receptor TrkB. BDNF is a well-recognized neurotrophic factor that regulates experience-dependent plasticity in different circuits in the brain. The internalization of the BDNF/TrkB complex results in signaling endosomes that allow local signaling in dendrites and presynaptic terminals, nuclear signaling in somas and dynein-mediated long-distance signaling from axons to cell bodies. In this review, we briefly discuss the organization of the endocytic pathway and how Rab11-recycling endosomes interact with other endomembrane systems. We further expand upon the roles of the Rab11-recycling pathway in neuronal plasticity. Then, we discuss the BDNF/TrkB signaling pathways and their functional relationships with the postendocytic trafficking of BDNF, including axonal transport, emphasizing the role of BDNF signaling endosomes, particularly Rab5-Rab11 endosomes, in neuronal plasticity. Finally, we discuss the evidence indicating that the dysfunction of the early-recycling pathway impairs BDNF signaling, contributing to several neurodegenerative diseases.
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.nbd.2022.105796
dc.identifier.eissn1095-953X
dc.identifier.issn0969-9961
dc.identifier.urihttps://doi.org/10.1016/j.nbd.2022.105796
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/93236
dc.identifier.wosidWOS:000822991200005
dc.language.isoen
dc.revistaNeurobiology of disease
dc.rightsacceso restringido
dc.subjectCentral nervous system
dc.subjectNeurons
dc.subjectDynein
dc.subjectRetrograde transport
dc.subjectRab5
dc.subjectRab11
dc.subjectEarly endosomes
dc.subjectRecycling endosomes
dc.subjectNeurotrophins
dc.subjectBDNF
dc.subjectTrkB
dc.subjectNeuronal plasticity
dc.subjectSignaling endosomes
dc.subjectNeurodegenerative diseases
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleThe Rab11-regulated endocytic pathway and BDNF/TrkB signaling: Roles in plasticity changes and neurodegenerative diseases
dc.typeartículo
dc.volumen171
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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