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The Atypical Antidepressant Tianeptine Confers Neuroprotection against Oxygen-Glucose Deprivation

ABSTRACT: The Atypical Antidepressant Tianeptine Confers Neuroprotection against Oxygen-Glucose Deprivation

PROVIDER: PRJNA983251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24908537.fastq.gz	Fastqsanger.gz
	SRR24908538.fastq.gz	Fastqsanger.gz
	SRR24908539.fastq.gz	Fastqsanger.gz
	SRR24908540.fastq.gz	Fastqsanger.gz
	SRR24908541.fastq.gz	Fastqsanger.gz

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The Atypical Antidepressant Tianeptine Confers Neuroprotection against Oxygen-Glucose Deprivation

Project description:Proregenerative and neuroprotective effects of antidepressants are an important topic of inquiry in neuropsychiatric research. Oxygen-glucose deprivation (OGD) mimics key aspects of ischemic injuryin vitro. Here, we studied the effects of 24-h pretreatment with serotonin (5-HT), citalopram (CIT), fluoxetine (FLU), and tianeptine (TIA) on primary mouse cortical neurons subjected to transient OGD. 5-HT (50 μM) statistically significantly enhanced neuron viability as measured by MTT assay and reduced cell death and LDH release. CIT (10 μM) and FLU (1 μM) did not increase the effects of 5-HT and neither antidepressant conferred neuroprotection in the absence of supplemental 5-HT in serum-free cell culture medium. By contrast, pre-treatment with TIA (10 μM) resulted in robust neuroprotection, even in the absence of 5-HT. Furthermore, TIA inhibited mRNA transcription of candidate genes related to cell death and hypoxia and attenuated lipid peroxidation, a hallmark of neuronal injury. Finally, deep RNA sequencing of primary neurons subjected to OGDdemonstrated that OGD induces many pathways relating to cell survival, the inflammation-immune response, synaptic dysregulation and apoptosis, andthatTIA pretreatment counteracted theseeffects of OGD. In conclusion, this study highlights the comparative strength of the 5-HT independent neuroprotective effects of TIA and identifies the molecular pathways involved.

2023-08-29 | GSE234798 | GEO

GPR56/ADGRG1 is associated with response to antidepressant treatment

Project description:It remains unclear why many patients with depression do not respond to antidepressant treatment. In three cohorts of individuals with depression and treated with serotonin-norepinephrine reuptake inhibitor (N=424) we show that responders, but not non-responders, display an increase of GPR56 mRNA in the blood. In a small group of subjects we also show that GPR56 is also downregulated in the PFC of individuals with depression that died by suicide. In mice, we show that chronic stress induced Gpr56 downregulation in the blood and prefrontal cortex (PFC), which is accompanied by depression-like behaviour, and can be reversed by antidepressant treatment. Gpr56 knockdown in mouse PFC was is associated with depressive-like behaviors, executive dysfunction and poor response to antidepressant treatment. GPR56 peptide agonists had antidepressant-like effects and up-regulated AKT/GSK3/EIF4 pathways. Our findings uncover a potential role of GPR56 in antidepressant response.

2020-03-31 | GSE146446 | GEO

Genetic determinants of antidepressant response

Project description:Genetic determinants of antidepressant response

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Genetic determinants of antidepressant response

Project description:Genetic determinants of antidepressant response

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miRNA profile of microglial cells under oxygen-glucose deprivation

2015-11-23 | GSE63504 | GEO

Treatment with antidepressant drugs in a rat model of Traumatic Brain Injury

Project description:Microarray analysis was performed to look at the mRNA and miRNA profiles of several antidepressant drugs in the rat hippocampus after Traumatic Brain Injury to test the hypothesis that antidepressant drugs ameliorate gene and miRNA dysregulation after TBI.

2019-05-01 | GSE115614 | GEO

Gene expression profile of microglial cells under oxygen-glucose deprivation

Project description:Migroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The mRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells.

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miRNA profile of microglial cells under oxygen-glucose deprivation

Project description:Migroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The miRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells. Two samples were analysed. miRNAs that were differentially expressed (increased or decreased in expression by â¥1.5-fold) between theOGD-activated and resting cells were identified.

2015-11-23 | E-GEOD-63504 | biostudies-arrayexpress

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Project description:The dentate gyrus (DG) of the hippocampus is one of major targets for antidepressant treatments. Our recent research has revealed that selective serotonin reuptake inhibitor (SSRI) treatment causes a long-lasting change in the phenotypes of mature dentate granule neurons to immature state in adult mouse DG. However, it is unknown whether this “dematuration” of DG is a common effect of antidepressant treatments and what mechanisms underlie it. Using electroconvulsive stimulation (ECS), a model of highly effective and fast-acting antidepressant therapy, here we show that neural stimulation via ECS induces rapid and lasting dematuration of granule neurons in DG. A single or few times of stimulation transiently reduced mature marker expression and mature synaptic functions. Repetitive stimulation converted this transient dematuration into a stable form lasting more than 1 month. Dematured granule neurons showed higher excitability, and an increase in GABA-mediated inhibition by the benzodiazepine diazepam prevented the lasting maintenance phase of dematuration without affecting the initial induction phase. Our study suggests that dematuration of DG is a common cellular mechanism underlying effects of different types of antidepressant treatments, and demonstrate a novel role for excitation/inhibition balance in bidirectional regulation of the state of neuronal maturation in the adult brain.

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