Genome Institute of Singapore, Agency for Science, Technology and Research (A*STAR), Singapore, 138672, Singapore.
Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montréal, H4H 1R3, QC, Canada.
Mol Psychiatry. 2022 Nov;27(11):4510-4525. doi: 10.1038/s41380-022-01725-1. Epub 2022 Sep 2.
Depression and anxiety are major global health burdens. Although SSRIs targeting the serotonergic system are prescribed over 200 million times annually, they have variable therapeutic efficacy and side effects, and mechanisms of action remain incompletely understood. Here, we comprehensively characterise the molecular landscape of gene regulatory changes associated with fluoxetine, a widely-used SSRI. We performed multimodal analysis of SSRI response in 27 mammalian brain regions using 310 bulk RNA-seq and H3K27ac ChIP-seq datasets, followed by in-depth characterisation of two hippocampal regions using single-cell RNA-seq (20 datasets). Remarkably, fluoxetine induced profound region-specific shifts in gene expression and chromatin state, including in the nucleus accumbens shell, locus coeruleus and septal areas, as well as in more well-studied regions such as the raphe and hippocampal dentate gyrus. Expression changes were strongly enriched at GWAS loci for depression and antidepressant drug response, stressing the relevance to human phenotypes. We observed differential expression at dozens of signalling receptors and pathways, many of which are previously unknown. Single-cell analysis revealed stark differences in fluoxetine response between the dorsal and ventral hippocampal dentate gyri, particularly in oligodendrocytes, mossy cells and inhibitory neurons. Across diverse brain regions, integrative omics analysis consistently suggested increased energy metabolism via oxidative phosphorylation and mitochondrial changes, which we corroborated in vitro; this may thus constitute a shared mechanism of action of fluoxetine. Similarly, we observed pervasive chromatin remodelling signatures across the brain. Our study reveals unexpected regional and cell type-specific heterogeneity in SSRI action, highlights under-studied brain regions that may play a major role in antidepressant response, and provides a rich resource of candidate cell types, genes, gene regulatory elements and pathways for mechanistic analysis and identifying new therapeutic targets for depression and anxiety.
抑郁和焦虑是全球主要的健康负担。尽管每年有超过 2 亿次处方使用针对血清素能系统的 SSRI,但它们的治疗效果和副作用各不相同,作用机制仍不完全清楚。在这里,我们全面描述了与广泛使用的 SSRI 氟西汀相关的基因调控变化的分子景观。我们使用 310 个批量 RNA-seq 和 H3K27ac ChIP-seq 数据集,对 27 个哺乳动物大脑区域的 SSRI 反应进行了多模态分析,随后使用单细胞 RNA-seq(20 个数据集)对两个海马区进行了深入表征。值得注意的是,氟西汀诱导了基因表达和染色质状态的深远的区域特异性变化,包括伏隔核壳、蓝斑核和隔区,以及更受关注的区域,如中缝核和海马齿状回。表达变化在与抑郁和抗抑郁药物反应相关的 GWAS 基因座中强烈富集,强调了与人类表型的相关性。我们观察到数十个信号受体和途径的差异表达,其中许多以前是未知的。单细胞分析显示,背侧和腹侧海马齿状回对氟西汀的反应存在明显差异,特别是在少突胶质细胞、苔藓细胞和抑制性神经元中。在不同的大脑区域,综合组学分析一致表明通过氧化磷酸化和线粒体变化增加能量代谢,我们在体外证实了这一点;因此,这可能构成氟西汀的共同作用机制。同样,我们观察到整个大脑普遍存在染色质重塑特征。我们的研究揭示了 SSRI 作用中意想不到的区域和细胞类型特异性异质性,突出了研究较少的大脑区域可能在抗抑郁反应中发挥主要作用,并提供了丰富的候选细胞类型、基因、基因调控元件和途径资源,用于机制分析和确定抑郁和焦虑的新治疗靶点。