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Transcriptome Alterations in ASMT Knockout-Induced Depression-Like Behaviors and Exercise Effects

ABSTRACT: Transcriptome Alterations in ASMT Knockout-Induced Depression-Like Behaviors and Exercise Effects

PROVIDER: PRJNA812598 | ENA |

REPOSITORIES: ENA

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Transcriptome Alterations in ASMT Knockout-Induced Depression-Like Behaviors and Exercise Effects

Project description:Sleep disorder caused by abnormal circadian rhythm is one of the main symptoms and risk factors of depression. N-acetylserotonin methyltransferase (ASMT), the last rate-limiting enzyme of melatonin (MT, a known hormone regulating circadian rhythms), has been reportedly associated with depression. Exercise can regulate circadian rhythm and play an important role in depression treatment. Recently, gene chip has been widely used in depression research. In the present study, we showed that ASMT knockout induced depression-like behaviors, which were ameliorated by swimming exercise. Moreover, swimming exercise increased serum levels of MT and 5-HT in ASMT knockout mice. In addition, transcriptome analysis identified 10 differentially expressed genes (DEGs) in KO mice compared with WT mice, and 29 DEGs in KO mice after swimming exercise. Among the DEGs, the direction and magnitude of change in Eps8l1 and Plcb2 were confirmed by qRT-PCR partly. Subsequent bioinformatic analysis showed that p53 signaling pathway, long-term depression and estrogen signaling pathway were enriched significantly. In the protein-protein interaction (PPI) networks, Mpp1 and Pidd1 were hub genes. These findings may provide new targets for the treatment of circadian rhythm-associated depression.

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The basolateral amygdala-anterior cingulate pathway contributes to depression-like behaviors and comorbidity with chronic pain behaviors in male mice

Project description:While depression and chronic pain are frequently comorbid, underlying neuronal circuits, and their relevance for the understanding of psychopathology, remain poorly defined. Here we show in mice that hyperactivity of the neuronal pathway linking the basolateral amygdala to the anterior cingulate cortex is essential for chronic pain-induced depression. In naive male mice, we demonstrate that activation of this pathway is sufficient to trigger depressive-like behaviors, as well as transcriptomic alterations that recapitulate core molecular features of depression in the human brain. These alterations notably impact gene modules related to myelination and the oligodendrocyte lineage. Among these, we show that Sema4a, a hub gene significantly upregulated in both male mice and humans in the context of altered mood, is necessary for the emergence of depressive-like behaviors. Overall, these results place the BLA-ACC pathway at the core of pain and depression comorbidity, and unravel the role of impaired myelination and Sema4a in mood control.

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A pancreas–hippocampus feedback mechanism regulates circadian changes in depression-related behaviors

Project description:Individuals with neuropsychiatric disorders often show metabolic symptoms. However, the mechanisms underlying this co-occurrence remain unclear. Here, we show that iPSC-derived pancreatic islets from individuals with bipolar disorder (BD) have insulin secretion deficits caused by increased expression of RORβ, a susceptibility gene for BD. Enhancing RORβ expression in mouse pancreatic β-cells induced depression-related behaviors in the light phase and mania-like behaviors in the dark phase. Pancreatic RORβ overexpression in the light phase reduced insulin release from islets, inducing hippocampal hyperactivity and depression-like behaviors. Further, this hippocampal hyperactivity in the light phase had the delayed effect of promoting insulin release in the dark phase, resulting mania-like behaviors and hippocampal neuronal hypoactivity. Our results in mice point to a pancreas–hippocampus feedback mechanism by which metabolic and circadian factors cooperate to generate behavioral fluctuations and which may play a role in bipolar disorder.

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Anterior cingulate cortex mediates the comorbidity between colorectal cancer and depression-like behaviors

Project description:In this study, we established mice with orthotopic colorectal cancer (CRC mice) and observed depression-like behaviors in the CRC mice. Through whole-brain c-FOS mapping, functional connectivity analysis, gut-brain inverse mapping, and correlation analysis, combined with chemogenetic manipulation, we identified the anterior cingulate cortex (ACC) as a key hub in the depression-related brain network. we performed whole transcriptome sequencing of key neural nuclei to identify molecular changes associated with CRC-depression comorbidity. Furthermore, chemogenetic modulation of neuronal excitability not only alleviated depression-like behavior but also reduced CRC progression in these mice. Importantly, our findings suggest that targeting the ACC, in addition to conventional colorectal cancer therapies, could offer therapeutic and quality-of-life benefits for patients with both CRC and depression.

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miR-17-92 cluster regulates adult hippocampal neurogenesis, anxiety and depression

Project description:Emerging evidence has shown that noncoding RNAs, particularly microRNAs (miRNAs), contribute to the pathogenesis of mood and anxiety disorders, although the molecular mechanisms are poorly understood. Here we show altered levels of miR-17-92 in adult hippocampal neural progenitors have a significant impact in neurogenesis and anxiety- and depression-related behaviors in mice. miR-17-92 deletion in adult neural progenitors causes a decrease, while its overexpression an increase of neurogenesis in the dentate gyrus, through regulating genes in the glucocorticoid pathway, especially serum- and glucocorticoid-inducible protein kinase-1 (Sgk1). miR-17-92 knockout mice show anxiety- and depression-like behaviors, whereas miR-17-92 overexpressing mice exhibit anxiolytic and antidepression-like behaviors. Furthermore, we show that miR-17-92 expression in the adult mouse hippocampus responds to chronic stress, and miR-17-92 rescues proliferation defects, induced by corticosterone, in hippocampal neural progenitors. Our study uncovers a crucial role for miR-17-92 in adult neural progenitors to regulate neurogenesis and anxiety- and depression-like behaviors.

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Project description:The increasing consumption of sugar-sweetened beverages (SSBs) in modern society has enhanced the epidemic of obesity, metabolic disorders, and mental illnesses. Therefore, the current study investigated the potential of 3M-Brazzein as a promising natural sugar substitute. 4-weeks-old leptin receptor knockout mice (db/db) were supplied with water, 10% sucrose solution, or a 3M-Brazzein solution respectively for 16 weeks. Chronic consumption of 3M-Brazzein did not cause any degeneration of adipogenesis, insulin resistance, hepatic lipogenesis, and depression-like behaviors. However, 10% sucrose consumed mice exhibited completely different outcomes. Furthermore, the mRNA expression levels of GLUT2, SREBF-1, and PPARγ in liver were significantly increased in knockout mice supplied with the 10% sucrose solution, thereby the excessive sucrose consumption induced severe obesity, impairment of glucose homeostasis, non-alcoholic fatty liver disease (NAFLD), and major depressive disorder in them. Consequently, the present study demonstrated the positive effects of 3M-Brazzein on various health problems prevalent in the modern world, and suggests some genetic clues related to the pathogenesis of NAFLD and major depressive disorder.

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The basolateral amygdala-anterior cingulate pathway contributes to depression-like behaviors and comorbidity with chronic pain behaviors in male mice

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Anterior cingulate cortex mediates the comorbidity between colorectal cancer and depression-like behaviors

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SARS-CoV-2 neurotropism induces anxiety/depression-like behaviors in mice [RNA-seq]

Project description:SARS-CoV-2 neurotropism induces anxiety/depression-like behaviors in mice [RNA-seq]

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