Down-Regulation of Decapping Protein 2 Mediates Chronic Nicotine Exposure-Induced Locomotor Hyperactivity in Drosophila
Guo, AK
刊名PLOS ONE
2012
卷号7期号:12页码:-e52521
关键词MESSENGER-RNA TURNOVER LONG-TERM CHANGES ADULT DROSOPHILA MELANOGASTER GENE RECEPTORS MODEL BEHAVIOR PATHWAY ETHANOL
ISSN号1932-6203
通讯作者Li, Y (reprint author), Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100080, Peoples R China.,liyan@ibp.ac.cn ; akguo@ion.ac.cn
英文摘要Long-term tobacco use causes nicotine dependence via the regulation of a wide range of genes and is accompanied by various health problems. Studies in mammalian systems have revealed some key factors involved in the effects of nicotine, including nicotinic acetylcholine receptors (nAChRs), dopamine and other neurotransmitters. Nevertheless, the signaling pathways that link nicotine-induced molecular and behavioral modifications remain elusive. Utilizing a chronic nicotine administration paradigm, we found that adult male fruit flies exhibited locomotor hyperactivity after three consecutive days of nicotine exposure, while nicotine-naive flies did not. Strikingly, this chronic nicotine-induced locomotor hyperactivity (cNILH) was abolished in Decapping Protein 2 or 1 (Dcp2 or Dcp1) -deficient flies, while only Dcp2-deficient flies exhibited higher basal levels of locomotor activity than controls. These results indicate that Dcp2 plays a critical role in the response to chronic nicotine exposure. Moreover, the messenger RNA (mRNA) level of Dcp2 in the fly head was suppressed by chronic nicotine treatment, and up-regulation of Dcp2 expression in the nervous system blocked cNILH. These results indicate that down-regulation of Dcp2 mediates chronic nicotine-exposure-induced locomotor hyperactivity in Drosophila. The decapping proteins play a major role in mRNA degradation; however, their function in the nervous system has rarely been investigated. Our findings reveal a significant role for the mRNA decapping pathway in developing locomotor hyperactivity in response to chronic nicotine exposure and identify Dcp2 as a potential candidate for future research on nicotine dependence.
学科主题Science & Technology - Other Topics
收录类别SCI
资助信息973 Program [2011CBA00400]; National Science Foundation of China [30921064, 90820008, 31130027, 31070956, 91132709]; One Hundred Talents Project of the CAS [KSCX2-YW-R-156]; "Strategic Priority Research Program" of the Chinese Academy of Sciences [XDB02040100]
语种英语
公开日期2013-06-04
内容类型期刊论文
源URL[http://ir.sibs.ac.cn/handle/331001/2478]  
专题上海神经科学研究所_神经所(总)
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Guo, AK. Down-Regulation of Decapping Protein 2 Mediates Chronic Nicotine Exposure-Induced Locomotor Hyperactivity in Drosophila[J]. PLOS ONE,2012,7(12):-e52521.
APA Guo, AK.(2012).Down-Regulation of Decapping Protein 2 Mediates Chronic Nicotine Exposure-Induced Locomotor Hyperactivity in Drosophila.PLOS ONE,7(12),-e52521.
MLA Guo, AK."Down-Regulation of Decapping Protein 2 Mediates Chronic Nicotine Exposure-Induced Locomotor Hyperactivity in Drosophila".PLOS ONE 7.12(2012):-e52521.
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