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Illumina 3'UTR biased-sequencing of total homogenate from mPFC and CeA of mice following chronic intermittent ethanol exposure and microglia depletion

ABSTRACT: Illumina 3'UTR biased-sequencing of total homogenate from mPFC and CeA of mice following chronic intermittent ethanol exposure and microglia depletion

PROVIDER: PRJNA597480 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10763812.fastq.gz	Fastqsanger.gz
	SRR10763813.fastq.gz	Fastqsanger.gz
	SRR10763814.fastq.gz	Fastqsanger.gz
	SRR10763815.fastq.gz	Fastqsanger.gz
	SRR10763816.fastq.gz	Fastqsanger.gz

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Illumina 3'UTR biased-sequencing of total homogenate from mPFC and CeA of mice following chronic intermittent ethanol exposure and microglia depletion

Project description:Purpose: Alcohol dependence results in microglia proliferation in brain and changes in microglia morphology and function. However, it remains unknown if microglia initiate or simply amplify the neuroadaptations that lead to alcohol dependence. Here we determined microglia function in chronic intermittent ethanol exposure behaviors using a colony stimulating factor 1 receptor inhibitor (PLX5622) and 3’UTR biased-sequencing. Therefore, the purpose of this study was to provide insight into how microglia may regulate neuroadaptations due to alcohol dependence. Methods: We performed 3’UTR biased transcriptome sequencing (3’Tag-seq) on total homogenate isolated from the prefrontal cortex (PFC) and central nucleus of the amygdala (CeA) of C57BL6/J mice following microglia depletion and chronic intermittent ethanol exposure. Results: Differential expression analysis and WGCNA network analysis revealed that microglia depletion prevents both immune and synaptic gene expression changes that are linked with the formation of alcohol dependence. This suggested that microglia are key regulators of the transition from alcohol misuse to alcohol dependence. Conclusion: Taken together our behavioral and transcriptional data indicate that microglia are the primary effector cell responsible for regulation of alcohol dependence. In addition, our data represents a novel resource for groups interested in transcriptional effects of microglia depletion after alcohol dependence.

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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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Glial transcriptome responses to chronic intermittent ethanol exposure

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