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Analysis of changes in transcriptomes of the rat medial prefrontal cortex tissues (mPFC) in vehicle group, chronic mild stress (CMS) group, and CMS+Phloretin group

ABSTRACT: Analysis of changes in transcriptomes of the rat medial prefrontal cortex tissues (mPFC) in vehicle group, chronic mild stress (CMS) group, and CMS+Phloretin group

PROVIDER: PRJNA795666 | ENA |

REPOSITORIES: ENA

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Analysis of changes in transcriptomes of the rat medial prefrontal cortex tissues (mPFC) in vehicle group, chronic mild stress (CMS) group, and CMS+Phloretin group

Project description:Purpose: The goals of this study are to investigate the effects of Phloretin (PHL) on the changes of genes in rat mPFC tissues between Vehicle group, CMS group, and CMS+PHL group. Methods: Vehicle group: Rats received vehicle by oral gavage for 2 weeks, and then were left undisturbed for 3 weeks except for necessary procedures, including handling and routine cleaning for 3 weeks. CMS group: Rats received vehicle by oral gavage for 2 weeks, and then were subjected to eight different stressors for 3 weeks in a random order, including foot shock, water deprivation, cold water swimming, food deprivation, restraint, clip tail, light/dark cycle reversal, and cage tilt. CMS+PHL group: Rats were pre-treated with 20 mg/kg. Phloretin for 2 weeks, and then exposed to above eight stressors randomly together with 20 mg/kg Phloretin for 3 weeks. In each group, we collected mPFC tissues from 3 rats and total RNA was extracted. RNA integrity was assessed using the RNA Nano 6000 Assay Kit of the Bioanalyzer 2100 system. The clustering of the index-coded samples was performed on a cBot Cluster Generation System using TruSeq PE Cluster Kit v3-cBot-HS (Illumina) according to the manufacturer’s instructions. After cluster generation, the library preparations were sequenced on an Illumina Novaseq platform and 150 bp paired-end reads were generated. Results: We found that Phloretin treatment changed some gene expression, especially in neuronal plasticity, compared with CMS group.

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Medial prefrontal cortex (mPFC) transcriptome analysis of Shank3-overexpressing mice

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Project description:The medial prefrontal cortex (mPFC) is critical for both the sensory and emotional /cognitive components of pain. However, the underlying mechanism still remains largely unknown. Here, we examined changes in the transciptomic profiles in the mPFC of mice with chronic pain using RNA sequencing (RNA-seq) technology. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different group of mPFC from mice, including ipsilateral part (Left side, the same to our operation part) of mPFC, contralateral part (Right side, opposite to our operation part) of mPFC after CCI (Chronic Constriction Injury of Sciatic Nerve) operation. Combining with naïve mice, at 28 days after operation.

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Project description:We investigated the methylated regions using MeDIP in naïve mice mPFC

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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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