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Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells

Rotenone is an inhibitor of mitochondrial complex I that produces a model of Parkinson’s disease (PD), in which neurons undergo dopamine release dysfunction and other features. In neurons, exocytosis is one of the processes associated with dopamine release and is dependent on Ca(2+) dynamic changes...

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Autores principales: Sai, Yan, Chen, Junfeng, Ye, Feng, Zhao, Yuanpeng, Zou, Zhongmin, Cao, Jia, Dong, Zhaojun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Japanese Society of Toxicologic Pathology 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3695337/
https://www.ncbi.nlm.nih.gov/pubmed/23914057
http://dx.doi.org/10.1293/tox.26.149
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author Sai, Yan
Chen, Junfeng
Ye, Feng
Zhao, Yuanpeng
Zou, Zhongmin
Cao, Jia
Dong, Zhaojun
author_facet Sai, Yan
Chen, Junfeng
Ye, Feng
Zhao, Yuanpeng
Zou, Zhongmin
Cao, Jia
Dong, Zhaojun
author_sort Sai, Yan
collection PubMed
description Rotenone is an inhibitor of mitochondrial complex I that produces a model of Parkinson’s disease (PD), in which neurons undergo dopamine release dysfunction and other features. In neurons, exocytosis is one of the processes associated with dopamine release and is dependent on Ca(2+) dynamic changes of the cell. In the present study, we have investigated the exocytosis of dopamine and the involvement of Ca(2+) in dopamine release in PC12 cells administrated with rotenone. Results demonstrated that rotenone led to an elevation of intracellular Ca(2+) through Ca(2+) influx by opening of the voltage-gated Ca(2+) channel and influenced the soluble N-ethylmaleimide attachment protein receptor (SNARE) proteins expression (including syntaxin, vesicle-associated membrane protein 2 (VAMP(2)) and synaptosome-associated protein 25 (SNAP-25)); pretreatment with a blocker of L-type voltage-activated Ca(2+) channels (nifedipine) decreased the intracellular dopamine levels and ROS formation, increased the cell viability and enhanced the neurite outgrowth and exocytosis of synaptic vesicles. These results indicated that the involvement of intracellular Ca(2+) was one of the factors resulting in suppression of dopamine release suppression in PC12 cells intoxicated with rotenone, which was associated with the rotenone-induced dopamine neurotoxicity.
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spelling pubmed-36953372013-08-02 Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells Sai, Yan Chen, Junfeng Ye, Feng Zhao, Yuanpeng Zou, Zhongmin Cao, Jia Dong, Zhaojun J Toxicol Pathol Original Article Rotenone is an inhibitor of mitochondrial complex I that produces a model of Parkinson’s disease (PD), in which neurons undergo dopamine release dysfunction and other features. In neurons, exocytosis is one of the processes associated with dopamine release and is dependent on Ca(2+) dynamic changes of the cell. In the present study, we have investigated the exocytosis of dopamine and the involvement of Ca(2+) in dopamine release in PC12 cells administrated with rotenone. Results demonstrated that rotenone led to an elevation of intracellular Ca(2+) through Ca(2+) influx by opening of the voltage-gated Ca(2+) channel and influenced the soluble N-ethylmaleimide attachment protein receptor (SNARE) proteins expression (including syntaxin, vesicle-associated membrane protein 2 (VAMP(2)) and synaptosome-associated protein 25 (SNAP-25)); pretreatment with a blocker of L-type voltage-activated Ca(2+) channels (nifedipine) decreased the intracellular dopamine levels and ROS formation, increased the cell viability and enhanced the neurite outgrowth and exocytosis of synaptic vesicles. These results indicated that the involvement of intracellular Ca(2+) was one of the factors resulting in suppression of dopamine release suppression in PC12 cells intoxicated with rotenone, which was associated with the rotenone-induced dopamine neurotoxicity. Japanese Society of Toxicologic Pathology 2013-07-10 2013-06 /pmc/articles/PMC3695337/ /pubmed/23914057 http://dx.doi.org/10.1293/tox.26.149 Text en ©2013 The Japanese Society of Toxicologic Pathology http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License.
spellingShingle Original Article
Sai, Yan
Chen, Junfeng
Ye, Feng
Zhao, Yuanpeng
Zou, Zhongmin
Cao, Jia
Dong, Zhaojun
Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells
title Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells
title_full Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells
title_fullStr Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells
title_full_unstemmed Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells
title_short Dopamine Release Suppression Dependent on an Increase of Intracellular Ca(2+) Contributed to Rotenone-induced Neurotoxicity in PC12 Cells
title_sort dopamine release suppression dependent on an increase of intracellular ca(2+) contributed to rotenone-induced neurotoxicity in pc12 cells
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3695337/
https://www.ncbi.nlm.nih.gov/pubmed/23914057
http://dx.doi.org/10.1293/tox.26.149
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