ArticleDiagnostic pathology2014
NF-κB signaling and vesicle transport are correlated with the reactivation of the memory trace of morphine dependence.
Article in Diagnostic pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Functional genomic mechanisms of opioid action and opioid use disorder: a systematic review of animal models and human studies.Molecular psychiatry · 2023Pooled it
- Review
- Stress- and drug-induced neuroimmune signaling as a therapeutic target for comorbid anxiety and substance use disorders.Pharmacology & therapeutics · 2022Review
- Gene Expression Profiling in the Striatum ofBiomolecules & therapeutics · 2021Article
- Morphine inhibits cell viability and growth via suppression of vascular endothelial growth factor in human oral cancer HSC-3 cells.Journal of anesthesia · 2019Article
- Requirement of NF-kappa B Activation in Different Mice Brain Areas during Long-Term Memory Consolidation in Two Contextual One-Trial Tasks with Opposing Valences.Frontiers in molecular neuroscience · 2017Article
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMorphine 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.
methodsMorphine 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.
resultsWe 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.
conclusionsThe 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. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1196707364133126.
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