附件1：征文要求.doc

附件1：征文要求 1、摘要论点明确、叙述清楚、文字精炼，限800字以内，包括题目、作者及单位、E-M地址。英文所有字体为Times New Roman；标题为号字加粗，署名小四号字，单位号字，正文五号字单倍行距。 2、请尽量提交近年来尚未发表的学术论文摘要。 3、请提供能反映您成就的个人资料（不超过00字）及近期照片。 4、本次会议采用邮件投稿，请将稿件统一发送至会务组邮箱：amhd@.。投稿截止日期：201年月日。 Decreased mitochondrial DNA copy number in the hippocampus and peripheral blood during opiate addiction is mediated by autophagy and can be salvaged by melatonin Yue-Mei Feng,1,2 Yun-Fang Jia,1,2 Ling-Yan Su,1,2 Dong Wang,1,2 Li Lv,1,2 Lin Xu1,* Yong-Gang Yao1,* 1Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences Yunnan Province; Kunming Institute of Zoology; Kunming, Yunnan China; 2University of Chinese Academy of Sciences; Beijing, China Abstract：Drug addiction is a chronic brain disease that is a serious social problem and causes enormous financial burden. Because mitochondrial abnormalities have been associated with opiate addiction, we examined the effect of morphine on mtDNA levels in rat and mouse models of addiction and in cultured cells. We found that mtDNA copy number was significantly reduced in the hippocampus and peripheral blood of morphine-addicted rats and mice compared with control animals. Concordantly, decreased mtDNA copy number and elevated mtDNA damage were observed in the peripheral blood from opiate-addicted patients, indicating detrimental effects of drug abuse and stress. In cultured rat pheochromocytoma (PC12) cells and mouse neurons, morphine treatment caused many mitochondrial defects, including a reduction in mtDNA copy number that was mediated by autophagy. Knockdown of the Atg7 gene was able to counteract the loss of mtDNA copy number induced by morphine. The mitochondria-targeted antioxidant melatonin restored mtDNA content and neuronal outgrowth and prevented the increase in autophagy upon morphine treatment. In mice, coadministration of melatonin with morphine ameliorated morphine-induced behavioral sensitization, analgesic tolerance and mtDNA content reduction. During drug withd