Suppr超能文献

可卡因和吗啡对伏隔核D1和D2中等多棘神经元的共享和不同转录组调控

Shared and divergent transcriptomic regulation in nucleus accumbens D1 and D2 medium spiny neurons by cocaine and morphine.

作者信息

Browne Caleb J, Mews Philipp, Zhou Xianxiao, Holt Leanne M, Estill Molly, Futamura Rita, Schaefer Anne, Kenny Paul J, Hurd Yasmin L, Shen Li, Zhang Bin, Nestler Eric J

机构信息

Nash Family Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai.

Dept. of Genetics and Genomic Sciences and Icahn Institute for Data Science and Genomic Technology, Icahn School of Medicine at Mount Sinai.

出版信息

bioRxiv. 2023 Sep 19:2023.09.19.558477. doi: 10.1101/2023.09.19.558477.

Abstract

Substance use disorders (SUDs) induce widespread molecular dysregulation in the nucleus accumbens (NAc), a brain region pivotal for coordinating motivation and reward. These molecular changes are thought to support lasting neural and behavioral disturbances that promote drug-seeking in addiction. However, different drug classes exert unique influences on neural circuits, cell types, physiology, and gene expression despite the overlapping symptomatology of SUDs. To better understand common and divergent molecular mechanisms governing SUD pathology, our goal was to survey cell-type-specific restructuring of the NAc transcriptional landscape in after psychostimulant or opioid exposure. We combined fluorescence-activated nuclei sorting and RNA sequencing to profile NAc D1 and D2 medium spiny neurons (MSNs) across cocaine and morphine exposure paradigms, including initial exposure, prolonged withdrawal after repeated exposure, and re-exposure post-withdrawal. Our analyses reveal that D1 MSNs display many convergent transcriptional responses across drug classes during exposure, whereas D2 MSNs manifest mostly divergent responses between cocaine and morphine, with morphine causing more adaptations in this cell type. Utilizing multiscale embedded gene co-expression network analysis (MEGENA), we discerned transcriptional regulatory networks subserving biological functions shared between cocaine and morphine. We observed largely integrative engagement of overlapping gene networks across drug classes in D1 MSNs, but opposite regulation of key D2 networks, highlighting potential therapeutic gene network targets within MSNs. These studies establish a landmark, cell-type-specific atlas of transcriptional regulation induced by cocaine and by morphine that can serve as a foundation for future studies towards mechanistic understanding of SUDs. Our findings, and future work leveraging this dataset, will pave the way for the development of targeted therapeutic interventions, addressing the urgent need for more effective treatments for cocaine use disorder and enhancing the existing strategies for opioid use disorder.

摘要

物质使用障碍(SUDs)会在伏隔核(NAc)中引发广泛的分子失调,伏隔核是协调动机和奖赏的关键脑区。这些分子变化被认为会导致持久的神经和行为紊乱,从而促使成瘾者寻求药物。然而,尽管物质使用障碍有重叠的症状,但不同类别的药物对神经回路、细胞类型、生理学和基因表达有独特的影响。为了更好地理解控制物质使用障碍病理的共同和不同分子机制,我们的目标是研究精神兴奋剂或阿片类药物暴露后伏隔核转录图谱的细胞类型特异性重组。我们结合荧光激活细胞核分选和RNA测序,对可卡因和吗啡暴露范式下的伏隔核D1和D2中型多棘神经元(MSNs)进行分析,包括初次暴露、重复暴露后的长期戒断以及戒断后的再次暴露。我们的分析表明,D1 MSNs在暴露期间对不同药物类别表现出许多趋同的转录反应,而D2 MSNs在可卡因和吗啡之间大多表现出不同的反应,吗啡在这种细胞类型中引起更多的适应性变化。利用多尺度嵌入式基因共表达网络分析(MEGENA),我们识别出了可卡因和吗啡共有的生物功能所对应的转录调控网络。我们观察到D1 MSNs中不同药物类别之间重叠基因网络的整合参与程度较高,但关键D2网络的调控相反,这突出了MSNs内潜在的治疗性基因网络靶点。这些研究建立了一个具有里程碑意义的、可卡因和吗啡诱导的转录调控细胞类型特异性图谱,可为未来对物质使用障碍进行机制理解的研究奠定基础。我们的发现以及利用该数据集的未来工作,将为靶向治疗干预措施的开发铺平道路,满足对可卡因使用障碍更有效治疗的迫切需求,并加强现有的阿片类药物使用障碍治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7034/10541108/c6f25327e37b/nihpp-2023.09.19.558477v1-f0001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验