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. 2017 Feb 28;10:49. doi: 10.3389/fnmol.2017.00049

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Copyright © 2017 Xue, Shi, Chen, Hang, Xia, Wu, Tao, Zhou, Shi and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Melatonin ameliorates KA-induced mitochondrial fragmentation and dysfunction. (A) Transmission electron microscope images of mitochondrial ultrastructure in KA and/or melatonin-treated N2a cells. (B) The morphology of mitochondria stained by mito-tracker in KA and/or melatonin-treated N2a cells. (C) Numbers of mitochondria in KA and/or melatonin-treated N2a cells. (D) Average length of mitochondria in KA and/or melatonin-treated N2a cells. (E) Mitochondrial membrane potential (MMP) in KA and/or melatonin-treated N2a cells. (F) ROS production in KA and/or melatonin-treated N2a cells. (G) ATP concentration in KA and/or melatonin-treated N2a cells (^∗∗P < 0.01 vs. controls; ^##P < 0.01 vs. the KA group; significant difference from the respective values determined by one-way analysis of variance test. n = 3).