Developmental axon degeneration requires trpv1-dependent Ca 2+ influx

Autores
Johnstone, Aaron D.; de Léon, Andrés; Unsain, Nicolas; Gibon, Julien; Barker, Philip A.
Año de publicación
2019
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Development of the nervous system relies on a balance between axon and dendrite growth and subsequent pruning and degeneration. The developmental degeneration of dorsal root ganglion (DRG) sensory axons has been well studied in part because it can be readily modeled by removing the trophic support by nerve growth factor (NGF) in vitro. We have recently reported that axonal fragmentation induced by NGF withdrawal is dependent on Ca2+, and here, we address the mechanism of Ca2+ entry required for developmental axon degeneration of mouse embryonic DRG neurons. Our results show that the transient receptor potential vanilloid family member 1 (TRPV1) cation channel plays a critical role mediating Ca2+ influx in DRG axons withdrawn from NGF. We further demonstrate that TRPV1 activation is dependent on reactive oxygen species (ROS) generation that is driven through protein kinase C (PKC) and NADPH oxidase (NOX)-dependent pathways that become active upon NGF withdrawal. These findings demonstrate novel mechanistic links between NGF deprivation, PKC activation, ROS generation, and TRPV1-dependent Ca2+ influx in sensory axon degeneration.
Fil: Johnstone, Aaron D.. University of British Columbia; Canadá. McGill University; Canadá
Fil: de Léon, Andrés. University of British Columbia; Canadá. McGill University; Canadá
Fil: Unsain, Nicolas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina
Fil: Gibon, Julien. University of British Columbia; Canadá
Fil: Barker, Philip A.. University of British Columbia; Canadá
Materia
NGF
TRKA
NEURODEGENERATION
PRUNING
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/121438
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/121438
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Developmental axon degeneration requires trpv1-dependent Ca 2+ influxJohnstone, Aaron D.de Léon, AndrésUnsain, NicolasGibon, JulienBarker, Philip A.NGFTRKANEURODEGENERATIONPRUNINGhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Development of the nervous system relies on a balance between axon and dendrite growth and subsequent pruning and degeneration. The developmental degeneration of dorsal root ganglion (DRG) sensory axons has been well studied in part because it can be readily modeled by removing the trophic support by nerve growth factor (NGF) in vitro. We have recently reported that axonal fragmentation induced by NGF withdrawal is dependent on Ca2+, and here, we address the mechanism of Ca2+ entry required for developmental axon degeneration of mouse embryonic DRG neurons. Our results show that the transient receptor potential vanilloid family member 1 (TRPV1) cation channel plays a critical role mediating Ca2+ influx in DRG axons withdrawn from NGF. We further demonstrate that TRPV1 activation is dependent on reactive oxygen species (ROS) generation that is driven through protein kinase C (PKC) and NADPH oxidase (NOX)-dependent pathways that become active upon NGF withdrawal. These findings demonstrate novel mechanistic links between NGF deprivation, PKC activation, ROS generation, and TRPV1-dependent Ca2+ influx in sensory axon degeneration.Fil: Johnstone, Aaron D.. University of British Columbia; Canadá. McGill University; CanadáFil: de Léon, Andrés. University of British Columbia; Canadá. McGill University; CanadáFil: Unsain, Nicolas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; ArgentinaFil: Gibon, Julien. University of British Columbia; CanadáFil: Barker, Philip A.. University of British Columbia; CanadáSociety for Neuroscience2019-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/121438Johnstone, Aaron D.; de Léon, Andrés; Unsain, Nicolas; Gibon, Julien; Barker, Philip A.; Developmental axon degeneration requires trpv1-dependent Ca 2+ influx; Society for Neuroscience; eNeuro; 6; 1; 1-2019; 1-152373-2822CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://eneuro.org/lookup/doi/10.1523/ENEURO.0019-19.2019info:eu-repo/semantics/altIdentifier/doi/10.1523/ENEURO.0019-19.2019info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-17T11:50:21Zoai:ri.conicet.gov.ar:11336/121438instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-17 11:50:22.216CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
title Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
spellingShingle Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
Johnstone, Aaron D.
NGF
TRKA
NEURODEGENERATION
PRUNING
title_short Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
title_full Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
title_fullStr Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
title_full_unstemmed Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
title_sort Developmental axon degeneration requires trpv1-dependent Ca 2+ influx
dc.creator.none.fl_str_mv Johnstone, Aaron D.
de Léon, Andrés
Unsain, Nicolas
Gibon, Julien
Barker, Philip A.
author Johnstone, Aaron D.
author_facet Johnstone, Aaron D.
de Léon, Andrés
Unsain, Nicolas
Gibon, Julien
Barker, Philip A.
author_role author
author2 de Léon, Andrés
Unsain, Nicolas
Gibon, Julien
Barker, Philip A.
author2_role author
author
author
author
dc.subject.none.fl_str_mv NGF
TRKA
NEURODEGENERATION
PRUNING
topic NGF
TRKA
NEURODEGENERATION
PRUNING
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Development of the nervous system relies on a balance between axon and dendrite growth and subsequent pruning and degeneration. The developmental degeneration of dorsal root ganglion (DRG) sensory axons has been well studied in part because it can be readily modeled by removing the trophic support by nerve growth factor (NGF) in vitro. We have recently reported that axonal fragmentation induced by NGF withdrawal is dependent on Ca2+, and here, we address the mechanism of Ca2+ entry required for developmental axon degeneration of mouse embryonic DRG neurons. Our results show that the transient receptor potential vanilloid family member 1 (TRPV1) cation channel plays a critical role mediating Ca2+ influx in DRG axons withdrawn from NGF. We further demonstrate that TRPV1 activation is dependent on reactive oxygen species (ROS) generation that is driven through protein kinase C (PKC) and NADPH oxidase (NOX)-dependent pathways that become active upon NGF withdrawal. These findings demonstrate novel mechanistic links between NGF deprivation, PKC activation, ROS generation, and TRPV1-dependent Ca2+ influx in sensory axon degeneration.
Fil: Johnstone, Aaron D.. University of British Columbia; Canadá. McGill University; Canadá
Fil: de Léon, Andrés. University of British Columbia; Canadá. McGill University; Canadá
Fil: Unsain, Nicolas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina
Fil: Gibon, Julien. University of British Columbia; Canadá
Fil: Barker, Philip A.. University of British Columbia; Canadá
description Development of the nervous system relies on a balance between axon and dendrite growth and subsequent pruning and degeneration. The developmental degeneration of dorsal root ganglion (DRG) sensory axons has been well studied in part because it can be readily modeled by removing the trophic support by nerve growth factor (NGF) in vitro. We have recently reported that axonal fragmentation induced by NGF withdrawal is dependent on Ca2+, and here, we address the mechanism of Ca2+ entry required for developmental axon degeneration of mouse embryonic DRG neurons. Our results show that the transient receptor potential vanilloid family member 1 (TRPV1) cation channel plays a critical role mediating Ca2+ influx in DRG axons withdrawn from NGF. We further demonstrate that TRPV1 activation is dependent on reactive oxygen species (ROS) generation that is driven through protein kinase C (PKC) and NADPH oxidase (NOX)-dependent pathways that become active upon NGF withdrawal. These findings demonstrate novel mechanistic links between NGF deprivation, PKC activation, ROS generation, and TRPV1-dependent Ca2+ influx in sensory axon degeneration.
publishDate 2019
dc.date.none.fl_str_mv 2019-01
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/121438
Johnstone, Aaron D.; de Léon, Andrés; Unsain, Nicolas; Gibon, Julien; Barker, Philip A.; Developmental axon degeneration requires trpv1-dependent Ca 2+ influx; Society for Neuroscience; eNeuro; 6; 1; 1-2019; 1-15
2373-2822
CONICET Digital
CONICET
url http://hdl.handle.net/11336/121438
identifier_str_mv Johnstone, Aaron D.; de Léon, Andrés; Unsain, Nicolas; Gibon, Julien; Barker, Philip A.; Developmental axon degeneration requires trpv1-dependent Ca 2+ influx; Society for Neuroscience; eNeuro; 6; 1; 1-2019; 1-15
2373-2822
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://eneuro.org/lookup/doi/10.1523/ENEURO.0019-19.2019
info:eu-repo/semantics/altIdentifier/doi/10.1523/ENEURO.0019-19.2019
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Society for Neuroscience
publisher.none.fl_str_mv Society for Neuroscience
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1843606851007021056
score 13.001348

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