1. Nicotine Modulates Mitochondrial Dynamics in Hippocampal Neurons
- Author
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Nibaldo C. Inestrosa, Juan A. Godoy, and Ángel G. Valdivieso
- Subjects
Dynamins ,0301 basic medicine ,Cell physiology ,Nicotine ,MITOCONDRIAS ,DPR1 ,Neuroscience (miscellaneous) ,Mitochondrion ,Biology ,Hippocampus ,Mitochondrial Dynamics ,Neuroprotection ,Rats, Sprague-Dawley ,NICOTINA ,Ciencias Biológicas ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,NICOTINE ,Animals ,Inositol 1,4,5-Trisphosphate Receptors ,Phosphorylation ,NEURONS ,Cells, Cultured ,Cytoskeleton ,Neurons ,NEURONAS ,MITOCHONDRIAL DYNAMICS ,Endoplasmic reticulum ,PGC-1Α ,Inositol trisphosphate receptor ,Bioquímica y Biología Molecular ,Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ,Cell biology ,Nicotinic acetylcholine receptor ,030104 developmental biology ,Neurology ,Mitochondrial biogenesis ,Energy source ,HIPOCAMPO ,030217 neurology & neurosurgery ,CIENCIAS NATURALES Y EXACTAS - Abstract
Fil: Godoy, Juan A. Pontificia Universidad Católica de Chile. Facultad de Ciencias Biológicas. Departamento de Biología Celular y Molecular. Centro de Envejecimiento y Regeneración; Cihle Fil: Godoy, Juan A. Universidad de Magallanes. Centro de Excelencia en Biomedicina de Magallanes; Chile Fil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Biología Celular y Molecular; Argentina Investigaciones Biomédicas. Laboratorio de Fil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Inestrosa, Nibaldo C. Pontificia Universidad Católica de Chile. Facultad de Ciencias Biológicas. Departamento de Biología Celular y Molecular. Centro de Envejecimiento y Regeneración; Cihle Fil: Inestrosa, Nibaldo C. Universidad de Magallanes. Centro de Excelencia en Biomedicina de Magallanes; Chile Fil: Inestrosa, Nibaldo C. University of New South Wales. Faculty of Medicine. School of Psychiatry. Centre for Healthy Brain Ageing; Australia Fil: Inestrosa, Nibaldo C. Pontificia Universidad Católica de Chile. Biomedical Center; Chile Abstract: 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.
- Published
- 2018