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Transcriptome analysis of microglia isolated from the mPFC or NAc without or with repeated social defeat stress (R-SDS)

ABSTRACT: To identify R-SDS-induced changes in gene expression profiles in medial prefrontal cortex (mPFC) and nucleus accumbens (NAc) microglia, we performed transcriptome analysis in mPFC and NAc microglia without or with R-SDS. Based on our observation that TLR2/TLR4 mediate R-SDS-induced activation of mPFC microglia, we performed the analysis in wild-type (WT) mice and TLR2/TLR4-double knockout (TLR-DKO) mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE115995 | GEO | 2018/08/09

REPOSITORIES: GEO

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Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in the medial prefrontal cortex (mPFC)

Project description:To identify R-SDS-induced changes in gene expression profiles in the mPFC, we performed transcriptome analysis in the mPFC without or with R-SDS. We separately analyzed the data from susceptible mice, which showed social avoidance after R-SDS, and resilient mice, which did not, in addition to those from naïve mice.

2018-08-09 | GSE115994 | GEO

Transcriptome analysis of microglia isolated from the mPFC or NAc without or with repeated social defeat stress (R-SDS)

Project description:Transcriptome analysis of microglia isolated from the mPFC or NAc without or with repeated social defeat stress (R-SDS)

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VTA and NAC labeled ribosome from mPFC

Project description:Projection-dependent ribosome profling from mouse mPFC. Ribosome from NAC- and VTA- projecting mPFC cells were immunoprecipited using GFP-trap (Chromotech). Translating mRNA was isolated and analyzed

2017-09-15 | GSE101185 | GEO

Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in the medial prefrontal cortex (mPFC)

Project description:Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in the medial prefrontal cortex (mPFC)

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Glucosylceramide fed mice skin before SDS treatment (0d), after SDS treatment (2d)

Project description:Dietary glucosylceramide (GC) improves skin barrier function. To elucidate the molecular mechanisms involved, we used a microarray system to analyze mRNA expression in SDS-treated dorsal skin of hairless mouse. Transepidermal water loss of mouse skin was increased by SDS treatment and the increase was significantly reduced by prior oral administration of glucosylceramides. Microarray-evaluated mRNA expression ratios showed statistically significant increase of expression of genes related to cornified envelope and tight junction formation versus all genes in glucosylceramide-fed/SDS-treated mouse skin. We then examined the contribution of glucosylceramide metabolites to tight junction formation of cultured keratinocytes. SDS treatment of cultured keratinocytes significantly decreased the transepidermal electrical resistance, and the decrease was significantly ameliorated in the presence of sphingosine or phytosphingosine, the major metabolites of glucosylceramide. These results suggest that oral administration of glucosylceramide improves skin barrier function by upregulating genes associated with both cornified envelope and tight junction formation.

2012-04-01 | GSE28086 | GEO

A genetically defined mPFC-thalamic circuit underlies pain chronicity

Project description:Chronic pain is a major health care problem with great social and economic consequences. Although the medial prefrontal cortex (mPFC) and the thalamus have been implicated in regulating pain, whether and how these regions may involve in pain chronification process have remained largely unknown. Here, we show that Foxp2+ neurons in mPFC, which are corticothalamic (CT) neurons representing the major mPFC output to thalamus, are deactivated in chronic inflammatory pain. Interestingly, prolonged, but not short-term, inactivation of the Foxp2+ neurons in mPFC increases the sensitivity to noxious stimulations. Conversely, chemogenetic activation of this neuronal cluster induces robust antinociceptive effects in both naïve mice and mice with chronic inflammatory pain. Furthermore, we found that the mPFC Foxp2+ neurons project to several thalamic relay nuclei and that activation of the mPFC to the parataenial nucleus of thalamus (PTN) circuit relieves pain. Finally, RNA-seq of the mPFC Foxp2+ neurons revealed that many genes related to neuronal activity are dysregulated in mice with chronic inflammatory pain. Collectively, our studies revealed that Foxp2+ neurons in mPFC that project to thalamus play a critical role in somatosensory processing and pain chronification.

2023-09-16 | GSE243136 | GEO

Proximity labeling proteomics reveals Kv1.3 potassium channel immune interactors in microglia.

Project description:Microglia are resident immune cells of the brain and regulate its inflammatory state. In neurodegenerative diseases, microglia transition from a homeostatic state to a state referred to as disease associated microglia (DAM). DAM express higher levels of proinflammatory signaling molecules, like STAT1 and TLR2, and show transitions in mitochondrial activity toward a more glycolytic response. Inhibition of Kv1.3 decreases the proinflammatory signature of DAM, though how Kv1.3 influences the response is unknown. Our goal was to establish the potential proteins interacting with Kv1.3 during transition to DAM. We utilized TurboID, a biotin ligase, fused to Kv1.3 to evaluate the potential interacting proteins with Kv1.3 via mass spectrometry in BV-2 microglia following TLR4-mediated activation. Electrophysiology, western blotting, and flow cytometry were used to evaluate Kv1.3 channel presence and TurboID biotinylation activity. We hypothesized that Kv1.3 contains domain-specific interactors that vary during a TLR4-induced inflammatory response, some of which are dependent on the PDZ-binding domain on the C-terminus. We determined that the N-terminus of Kv1.3 is responsible for trafficking Kv1.3 to the cell surface and mitochondria (e.g. NUNDC, TIMM50). Whereas, the C-terminus interacts with immune signaling proteins in an LPS-induced inflammatory response (e.g. STAT1, TLR2, and C3). There are 70 proteins that rely on the C-terminal PDZ-binding domain to interact with Kv1.3 (e.g. ND3, Snx3, and Sun1). Overall, we highlight that the Kv1.3 potassium channel functions beyond conducting the outward flux of potassium ions in an inflammatory context and that KV1.3 modulates activity of key immune signaling proteins, such as STAT1 and C3

2024-05-06 | PXD049433 | Pride

Dysfunction of the NAc-mPFC circuit in insomnia disorder.

Project description:BackgroundInsomnia disorder (ID) is a prevalent sleep disorder, which seriously affects people's daily life and was found to be associated with increased frequency of sleep stage shifts. Previous findings had revealed the critical role of the nucleus accumbens (NAc) in sleep-wake transition. However, the neuroimaging studies of the NAc in patients with ID have been rare. We hypothesized that structural and functional abnormalities of the NAc would be implicated in ID.MethodsTwenty-six ID patients and 36 matched healthy controls (HC) were included in the current study. The volumes and corresponding resting-state functional connectivity (RSFC) of the bilateral NAc were compared between the two groups. The abnormal RSFC in ID were then correlated with Pittsburgh Sleep Quality Index (PSQI).ResultsCompared with HC, ID patients showed significantly increased volume of right NAc. Several brain regions showed increased RSFC with the NAc in ID patients, such as medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), caudate and putamen. Meanwhile, the occipital gyrus and temporal gyrus showed decreased RSFC with the NAc. Additionally, the increased RSFC strength between bilateral NAc and left mPFC was significant correlated with PSQI scores in ID patients.ConclusionDysfunctions of the NAc-mPFC circuit were found in ID patients, which were associated with sleep quality measured by PSQI. The two patterns of increase and decrease of RSFC in ID patients observed in our study may reflect the state of hyperarousal and potential impairment of cognitive function in the patients, respectively. It is hoped that our study focusing on NAc-mPFC circuits could provide new insights for the neural mechanisms of ID and potential novel therapeutic targets for treatment of ID patients.

| S-EPMC7606871 | biostudies-literature

Glucosylceramide fed mice skin before SDS treatment (0d), after SDS treatment (2d)

2012-03-31 | E-GEOD-28086 | biostudies-arrayexpress

Expression data from Drd2+ cells of mouse mPFC

Project description:The heterogeneity of cortical dopamine D2 receptor expressing cells is not well characterized We performed microarrays to study expression of all the transcriprts specifically from Drd2+ neurons of mouse mPFC. For this we immunoprecipitated ribosomes from mPFC of D2Cre::RiboTag mouse, where ribosomal subunit Rpl22 is tagged with HA epitope specifically in Drd2+ neurons

2018-06-16 | GSE115887 | GEO

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