title: NF-κB signaling and vesicle transport are correlated with the reactivation of the memory trace of morphine dependence.
abstract: BACKGROUND
  Morphine has been widely used as a clinical anesthetic and analgesic. However, abuse of morphine might result in psychological and physiological dependence. Previous studies have indicated that memory mechanisms play critical roles in morphine dependence.
  
  
  METHODS
  Morphine dependence was established in mice utilizing place preference conditioning (CPP). We observed changes in the methylome and transcriptome of the nucleus accumbens during the reactivation of the memory trace. We also monitored for changes in the methylome and transcriptome of mice that were acutely exposed to morphine.
  
  
  RESULTS
  We detected 165 and 18 differentially expressed genes (DEGs) and 6 and 24 significant methyl-sensitive cut counting (MSCC) windows in the acute morphine treatment and the CPP model, respectively. The changes in the methylome and transcriptome during the acute treatment were mainly caused by a response to the morphine stimulus; most of the DEGs were correlated with hormone or transcription factor activity regulation. The expression levels of Lcn2 and Hspb1, which participate in the activation of NF-κB, were significantly decreased in the CPP morphine treatment model. Besides, the alternative splicing of the curtailed isoform of Caps1 was significantly increased in the CPP morphine-treated group, and the methylation levels of Arf4, Vapa, and Gga3 were decreased. These genes play critical roles in the regulation of the Golgi network.
  
  
  CONCLUSIONS
  The current study indicates that NF-κB signaling and vesicular transport are correlated with the reactivation of the memory trace in morphine-dependent mice. The results obtained in our study agree with previous observations and identify additional candidate genes for further research.
  The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1196707364133126.
authors.forename: Junyi
authors.initials: J
authors.lastname: Ye
authors.forename: Zhaoyang
authors.initials: Z
authors.lastname: Yang
authors.forename: Candong
authors.initials: C
authors.lastname: Li
authors.forename: Meimei
authors.initials: M
authors.lastname: Cai
authors.forename: Daizhan
authors.initials: D
authors.lastname: Zhou
authors.forename: Qin
authors.initials: Q
authors.lastname: Zhang
authors.forename: Yiming
authors.initials: Y
authors.lastname: Wei
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.affiliation: Institute of Biomedical Sciences, Fudan University, Shanghai, PR China. superliuyun@gmail.com.
authors.forename: Yun
authors.initials: Y
authors.lastname: Liu
mesh_terms: D000818:Animals; D003214:Conditioning, Classical; D022162:Cytoplasmic Vesicles / Q000378:metabolism; D008297:Male; D008568:Memory / Q000502:physiology*; D051379:Mice; D009021:Morphine Dependence / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism; D009714:Nucleus Accumbens / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D021381:Protein Transport / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*; D059467:Transcriptome
chemical_list: D016328:NF-kappa B