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Title of Journal: Mol Cell Biochem

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Abbravation: Molecular and Cellular Biochemistry

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Springer US

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DOI

10.1016/0020-7403(73)90107-0

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ISSN

1573-4919

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CNTFACM promotes mitochondrial respiration and ox

Authors: Meiqun Sun Hongli Liu Huanbai Xu Hongtao Wang Xiaojing Wang
Publish Date: 2016/08/11
Volume: 420, Issue: 1-2, Pages: 195-206
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Abstract

A specialized culture medium termed ciliary neurotrophic factortreated astrocyteconditioned medium CNTFACM allows investigators to assess the peripheral effects of CNTFinduced activated astrocytes upon cultured neurons CNTFACM has been shown to upregulate neuronal Ltype calcium channel current activity which has been previously linked to changes in mitochondrial respiration and oxidative stress Therefore the aim of this study was to evaluate CNTFACM’s effects upon mitochondrial respiration and oxidative stress in rat cortical neurons Cortical neurons CNTFACM and untreated control astrocyteconditioned medium UCACM were prepared from neonatal Sprague–Dawley rat cortical tissue Neurons were cultured in either CNTFACM or UCACM for a 48h period Changes in the following parameters before and after treatment with the Ltype calcium channel blocker isradipine were assessed i intracellular calcium levels ii mitochondrial membrane potential ΔΨm iii oxygen consumption rate OCR and adenosine triphosphate ATP formation iv intracellular nitric oxide NO levels v mitochondrial reactive oxygen species ROS production and vi susceptibility to the mitochondrial complex I toxin rotenone CNTFACM neurons displayed the following significant changes relative to UCACM neurons i increased intracellular calcium levels p  005 ii elevation in ΔΨm p  005 iii increased OCR and ATP formation p  005 iv increased intracellular NO levels p  005 v increased mitochondrial ROS production p  005 and vi increased susceptibility to rotenone p  005 Treatment with isradipine was able to partially rescue these negative effects of CNTFACM p  005 CNTFACM promotes mitochondrial respiration and oxidative stress in cortical neurons through elevating Ltype calcium channel activityThis work was supported by the National Natural Science Foundation of China Grant No 81171117 the Doctor Point Foundation of the Chinese Ministry of Education Grant No 44 and the National Natural Science Foundation of Anhui Province Grant No 1506c085014

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