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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)

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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.

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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.

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

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Repeated social defeat stress (R-SDS)-induced changes in gene expression profiles in microglia or whole medial prefrontal cortex

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

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