Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons

Autores
Godoy, Juan A.; Valdivieso, Ángel Gabriel; Inestrosa, Nibaldo C.
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Mitochondria are widely recognized as fundamental organelles for cellular physiology and constitute the main energy source for different cellular processes. The location, morphology, and interactions of mitochondria with other organelles, such as the endoplasmic reticulum (ER), have emerged as critical events capable of determining cellular fate. Mitochondria-related functions have proven particularly relevant in neurons; mitochondria are necessary for proper neuronal morphogenesis and the highly energy-demanding synaptic transmission process. Mitochondrial health depends on balanced fusion-fission events, termed mitochondrial dynamics, to repair damaged organelles and/or improve the quality of mitochondrial function, ATP production, calcium homeostasis, and apoptosis, which represent some mitochondrial functions closely related to mitochondrial dynamics. Several neurodegenerative disorders, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, have been correlated with severe mitochondrial dysfunction. In this regard, nicotine, which has been associated with relevant neuroprotective effects mainly through activation of the nicotinic acetylcholine receptor (nAChR), exerts its effects at least in part by acting directly on mitochondrial physiology and morphology. Additionally, a recent description of mitochondrial nAChR localization suggests a nicotine-dependent mitochondrial function. In the present work, we evaluated in cultured hipocampal neurons the effects of nicotine on mitochondrial dynamics by assessing mitochondrial morphology, membrane potential, as well as interactions between mitochondria, cytoskeleton and IP3R, levels of the cofactor PGC-1α, and fission-fusion-related proteins. Our results suggest that nicotine modulates mitochondrial dynamics and influences mitochondrial association from microtubules, increasing IP3 receptor clustering showing modulation between mitochondria-ER communications, together with the increase of mitochondrial biogenesis.
Fil: Godoy, Juan A.. Universidad de Magallanes; Chile. Pontificia Universidad Catolica de Chile. Facultad de Ciencias Biológicas; Chile
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Inestrosa, Nibaldo C.. Universidad de Magallanes; Chile. University of New South Wales; Australia. Pontificia Universidad Catolica de Chile. Facultad de Ciencias Biológicas; Chile
Materia
DPR1
MITOCHONDRIAL DYNAMICS
NEURONS
NICOTINE
PGC-1Α
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:11336/98921
Acceder
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network_name_str CONICET Digital (CONICET)
spelling Nicotine Modulates Mitochondrial Dynamics in Hippocampal NeuronsGodoy, Juan A.Valdivieso, Ángel GabrielInestrosa, Nibaldo C.DPR1MITOCHONDRIAL DYNAMICSNEURONSNICOTINEPGC-1Αhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Mitochondria are widely recognized as fundamental organelles for cellular physiology and constitute the main energy source for different cellular processes. The location, morphology, and interactions of mitochondria with other organelles, such as the endoplasmic reticulum (ER), have emerged as critical events capable of determining cellular fate. Mitochondria-related functions have proven particularly relevant in neurons; mitochondria are necessary for proper neuronal morphogenesis and the highly energy-demanding synaptic transmission process. Mitochondrial health depends on balanced fusion-fission events, termed mitochondrial dynamics, to repair damaged organelles and/or improve the quality of mitochondrial function, ATP production, calcium homeostasis, and apoptosis, which represent some mitochondrial functions closely related to mitochondrial dynamics. Several neurodegenerative disorders, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, have been correlated with severe mitochondrial dysfunction. In this regard, nicotine, which has been associated with relevant neuroprotective effects mainly through activation of the nicotinic acetylcholine receptor (nAChR), exerts its effects at least in part by acting directly on mitochondrial physiology and morphology. Additionally, a recent description of mitochondrial nAChR localization suggests a nicotine-dependent mitochondrial function. In the present work, we evaluated in cultured hipocampal neurons the effects of nicotine on mitochondrial dynamics by assessing mitochondrial morphology, membrane potential, as well as interactions between mitochondria, cytoskeleton and IP3R, levels of the cofactor PGC-1α, and fission-fusion-related proteins. Our results suggest that nicotine modulates mitochondrial dynamics and influences mitochondrial association from microtubules, increasing IP3 receptor clustering showing modulation between mitochondria-ER communications, together with the increase of mitochondrial biogenesis.Fil: Godoy, Juan A.. Universidad de Magallanes; Chile. Pontificia Universidad Catolica de Chile. Facultad de Ciencias Biológicas; ChileFil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Inestrosa, Nibaldo C.. Universidad de Magallanes; Chile. University of New South Wales; Australia. Pontificia Universidad Catolica de Chile. Facultad de Ciencias Biológicas; ChileHumana Press2018-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/98921Godoy, Juan A.; Valdivieso, Ángel Gabriel; Inestrosa, Nibaldo C.; Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons; Humana Press; Molecular Neurobiology; 55; 12; 12-2018; 8965-89770893-7648CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s12035-018-1034-8info:eu-repo/semantics/altIdentifier/doi/10.1007/s12035-018-1034-8info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:43:44Zoai:ri.conicet.gov.ar:11336/98921instacron: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:34982025-09-29 09:43:45.064CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
title Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
spellingShingle Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
Godoy, Juan A.
DPR1
MITOCHONDRIAL DYNAMICS
NEURONS
NICOTINE
PGC-1Α
title_short Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
title_full Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
title_fullStr Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
title_full_unstemmed Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
title_sort Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
dc.creator.none.fl_str_mv Godoy, Juan A.
Valdivieso, Ángel Gabriel
Inestrosa, Nibaldo C.
author Godoy, Juan A.
author_facet Godoy, Juan A.
Valdivieso, Ángel Gabriel
Inestrosa, Nibaldo C.
author_role author
author2 Valdivieso, Ángel Gabriel
Inestrosa, Nibaldo C.
author2_role author
author
dc.subject.none.fl_str_mv DPR1
MITOCHONDRIAL DYNAMICS
NEURONS
NICOTINE
PGC-1Α
topic DPR1
MITOCHONDRIAL DYNAMICS
NEURONS
NICOTINE
PGC-1Α
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Mitochondria are widely recognized as fundamental organelles for cellular physiology and constitute the main energy source for different cellular processes. The location, morphology, and interactions of mitochondria with other organelles, such as the endoplasmic reticulum (ER), have emerged as critical events capable of determining cellular fate. Mitochondria-related functions have proven particularly relevant in neurons; mitochondria are necessary for proper neuronal morphogenesis and the highly energy-demanding synaptic transmission process. Mitochondrial health depends on balanced fusion-fission events, termed mitochondrial dynamics, to repair damaged organelles and/or improve the quality of mitochondrial function, ATP production, calcium homeostasis, and apoptosis, which represent some mitochondrial functions closely related to mitochondrial dynamics. Several neurodegenerative disorders, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, have been correlated with severe mitochondrial dysfunction. In this regard, nicotine, which has been associated with relevant neuroprotective effects mainly through activation of the nicotinic acetylcholine receptor (nAChR), exerts its effects at least in part by acting directly on mitochondrial physiology and morphology. Additionally, a recent description of mitochondrial nAChR localization suggests a nicotine-dependent mitochondrial function. In the present work, we evaluated in cultured hipocampal neurons the effects of nicotine on mitochondrial dynamics by assessing mitochondrial morphology, membrane potential, as well as interactions between mitochondria, cytoskeleton and IP3R, levels of the cofactor PGC-1α, and fission-fusion-related proteins. Our results suggest that nicotine modulates mitochondrial dynamics and influences mitochondrial association from microtubules, increasing IP3 receptor clustering showing modulation between mitochondria-ER communications, together with the increase of mitochondrial biogenesis.
Fil: Godoy, Juan A.. Universidad de Magallanes; Chile. Pontificia Universidad Catolica de Chile. Facultad de Ciencias Biológicas; Chile
Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
Fil: Inestrosa, Nibaldo C.. Universidad de Magallanes; Chile. University of New South Wales; Australia. Pontificia Universidad Catolica de Chile. Facultad de Ciencias Biológicas; Chile
description Mitochondria are widely recognized as fundamental organelles for cellular physiology and constitute the main energy source for different cellular processes. The location, morphology, and interactions of mitochondria with other organelles, such as the endoplasmic reticulum (ER), have emerged as critical events capable of determining cellular fate. Mitochondria-related functions have proven particularly relevant in neurons; mitochondria are necessary for proper neuronal morphogenesis and the highly energy-demanding synaptic transmission process. Mitochondrial health depends on balanced fusion-fission events, termed mitochondrial dynamics, to repair damaged organelles and/or improve the quality of mitochondrial function, ATP production, calcium homeostasis, and apoptosis, which represent some mitochondrial functions closely related to mitochondrial dynamics. Several neurodegenerative disorders, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, have been correlated with severe mitochondrial dysfunction. In this regard, nicotine, which has been associated with relevant neuroprotective effects mainly through activation of the nicotinic acetylcholine receptor (nAChR), exerts its effects at least in part by acting directly on mitochondrial physiology and morphology. Additionally, a recent description of mitochondrial nAChR localization suggests a nicotine-dependent mitochondrial function. In the present work, we evaluated in cultured hipocampal neurons the effects of nicotine on mitochondrial dynamics by assessing mitochondrial morphology, membrane potential, as well as interactions between mitochondria, cytoskeleton and IP3R, levels of the cofactor PGC-1α, and fission-fusion-related proteins. Our results suggest that nicotine modulates mitochondrial dynamics and influences mitochondrial association from microtubules, increasing IP3 receptor clustering showing modulation between mitochondria-ER communications, together with the increase of mitochondrial biogenesis.
publishDate 2018
dc.date.none.fl_str_mv 2018-12
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/11336/98921
Godoy, Juan A.; Valdivieso, Ángel Gabriel; Inestrosa, Nibaldo C.; Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons; Humana Press; Molecular Neurobiology; 55; 12; 12-2018; 8965-8977
0893-7648
CONICET Digital
CONICET
url http://hdl.handle.net/11336/98921
identifier_str_mv Godoy, Juan A.; Valdivieso, Ángel Gabriel; Inestrosa, Nibaldo C.; Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons; Humana Press; Molecular Neurobiology; 55; 12; 12-2018; 8965-8977
0893-7648
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s12035-018-1034-8
info:eu-repo/semantics/altIdentifier/doi/10.1007/s12035-018-1034-8
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 Humana Press
publisher.none.fl_str_mv Humana Press
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
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score 13.070432

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