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STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [RNA-Seq stress]

ABSTRACT: STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [RNA-Seq stress]

PROVIDER: PRJNA1155615 | ENA |

REPOSITORIES: ENA

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STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [RNA-Seq stress]

Project description:Acute stress can inhibit the activity of dopaminergic neurons in the ventral tegmental area (VTA), leading to increased anxiety and reduced sensitivity to natural rewards. However, the molecular mechanisms underlying this effect remain unclear. Our study shows that acute restraint stress increases the phosphorylation of the transcription factor STAT3 at Ser727 and Tyr705 in VTA dopaminergic neurons, enhancing its transcriptional activity. This modulation contributes to the inhibition of dopaminergic neuron activity, heightened anxiety, and reduced reward sensitivity. Furthermore, acute stress also promotes O-GlcNAcylation in VTA neurons, which competes with STAT3 Ser727 but not Tyr705 phosphorylation and modulates its transcriptional activity, leading to alterations in GABA receptor expression. This reveals a complex molecular feedback mechanism where O-GlcNAcylation regulates STAT3 activity to maintain brain homeostasis during acute stress responses.

2025-09-01 | GSE276173 | GEO

STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [ATAC-Seq]

2025-09-01 | GSE276171 | GEO

STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [RNA-Seq Ogt]

2025-09-01 | GSE276183 | GEO

STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition

2024-09-07 | PXD055720 |

STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [ATAC-Seq]

Project description:STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [ATAC-Seq]

| PRJNA1155620 | ENA

STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [RNA-Seq Ogt]

Project description:STAT3S727 Phosphorylation in VTA Dopaminergic Neurons Competed by O-GlcNAcylation Regulates Acute Stress-Induced Anxiety and Reward Inhibition [RNA-Seq Ogt]

| PRJNA1155652 | ENA

Persistent open chromatin state in early-life stress-activated cells of the VTA

Project description:Early-life stress sensitizes individuals to subsequent stressors to increase lifetime risk for psychiatric disorders. Within the ventral tegmental area (VTA), a mesolimbic brain region implicated in stress response and mental health, early-life stress causes long-lasting changes in gene expression and chromatin modifications that in turn cause latent physiological and behavioral sensitivity to stress. These molecular consequences of early-life stress are indicative of epigenetic priming, a form of molecular memory in which developmental or environmental cues open chromatin at enhancers to facilitate transcriptional response to stimuli. However, the long term impact of early-life stress on chromatin architecture in the VTA was not yet known. Using a combination of activity-dependent cellular tagging and ATAC-sequencing, we find that early-life stress opens chromatin specifically in stress-activated cells of the VTA, that this remodeling persists into adulthood, and that opening chromatin at cis-regulatory elements including enhancers augments transcriptional response to adult stress. Together, this data supports enhancer priming within ELS-responsive cells in the VTA as a biological mechanism for lifelong stress sensitivity.

2025-09-09 | GSE268468 | GEO

Sex-specific transcriptomic profiling of reward and sensory brain areas in perinatal fentanyl exposed juvenile mice+G4

Project description:Using bulk RNAseq, we explored transcriptomic landscape of three reward areas - PrL, NAc, VTA and two sensory areas -S1, VBT in perinatal fentanyl exposed juvenile mice

2023-05-08 | GSE231981 | GEO

Reward System Activation Improves Recovery from Acute Myocardial Infarction".

Project description:The recovery from acute myocardial infarction (AMI) is influenced by physiological and psychological factors. While the physiological effects have been extensively studied, the contribution of psychological factors and whether they can be modulated is not completely clear. Here we show that the activity of the reward system, a brain network involved in motivation and positive expectation, affects outcomes in mice following AMI. We found that chemogenetic activation of dopaminergic neurons in the ventral tegmental area (VTA) significantly attenuated the remodeling process following AMI, resulting in improved left-ventricular performance compared to controls. VTA activation was associated with modulation of the immune response following AMI and increased blood vessel formation in the damaged area, mediated, at least in part, by changes in liver-secreted proteins. Together, our findings reveal a potential mechanism by which specific brain activity can affect the multifactorial systemic and local tissue response to AMI, introducing a novel target for therapeutic interventions

2024-05-03 | PXD043448 | Pride

Chronic stress deficits in reward behaviour co-occur with low nucleus accumbens dopamine activity during reward anticipation specifically

Project description:Whilst reward pathologies e.g., anhedonia and apathy, are major and common in stress-related neuropsychiatric disorders, their neurobiological bases and therefore treatment are poorly understood. Functional imaging studies in humans with reward pathology indicate that attenuated BOLD activity in nucleus accumbens (NAc) occurs during reward anticipation/expectancy but not reinforcement; potentially, this is dopamine (DA) related. In mice, chronic social stress (CSS) leads to reduced reward learning and effortful motivation and, here, DA-sensor fibre photometry was used to investigate whether these behavioural deficits co-occur with altered NAc DA activity during reward anticipation and/or reinforcement. In CSS mice relative to controls: (1) Reduced discriminative learning of the sequence, tone-on + appetitive behaviour = tone-on + sucrose reinforcement, co-occurred with attenuated NAc DA activity throughout tone-on and sucrose reinforcement. (2) Reduced effortful motivation during the sequence, operant behaviour = tone-on + sucrose delivery + tone-off / appetitive behaviour = sucrose reinforcement, co-occurred with attenuated NAc DA activity at tone-on and typical activity at sucrose reinforcement. (3) Reduced effortful motivation during the sequence, operant behaviour = appetitive behaviour + sociosexual reinforcement co-occurred with typical NAc DA activity at female reinforcement. Therefore, in CSS mice attenuated NAc DA activity is specific to reward anticipation and as such potentially causal to deficits in learning and motivation. CSS did not impact on the transcriptome of ventral tegmentum DA neurons, suggesting that its stimulus-specific effects on NAc DA activity originate elsewhere in the neural circuitry of reward processing.

2024-07-31 | GSE268460 | GEO

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