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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/98921
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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 Técnicas2025-09-03T09:49:39Zoai: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:34982025-09-03 09:49:40.087CONICET 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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1842268986473971712 |
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13.13397 |