Morphine incubation craving-NAc_small RNA sequencing
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ABSTRACT:
PROVIDER: PRJNA793681 | ENA |
REPOSITORIES: ENA
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Project description:The current study aimed at addressing two questions: 1) How the expression of key miRNAs is altered in the NAc during the cue-induced incubation of morphine craving? 2) Which is/are the target gene(s) and what is/are the regulatory mechanism(s) of gene(s) in response to the candidate miRNAs? To answer these two questions, the cue-induced incubation of the morphine craving model was first established by using the conditioned place preference (CPP) paradigm. Then, the aberrant expression of miRNAs was identified in the NAc tissue by RNA-sequencing.
2022-06-08 | GSE192888 | GEO
Project description:The current study aimed at addressing two questions: 1) How the expression of key miRNAs is altered in the NAc during the morphine-induced addiction? 2) Which is/are the target gene(s) and what is/are the regulatory mechanism(s) of gene(s) in response to the candidate miRNAs? To answer these two questions, the morphine addiction model was first established by using the conditioned place preference (CPP) paradigm. Then, the aberrant expression of miRNAs was identified in the NAc tissue by RNA-sequencing.
2022-04-04 | GSE199917 | GEO
Project description:Morphine addiction-NAc_small RNA sequencing
| PRJNA822089 | ENA
Project description:The current study aimed at addressing two questions: 1) How the expression of key lncRNAs is altered in the NAc during the morphine-induced addiction? 2) Which is/are the target gene(s) and what is/are the regulatory mechanism(s) of gene(s) in response to the candidate lncRNAs? To answer these two questions, the morphine addiction model was first established by using the conditioned place preference (CPP) paradigm. Then, the aberrant expression of lncRNAs was identified in the NAc tissue by RNA-sequencing.
2022-04-09 | GSE200282 | GEO
Project description:The current study aimed at addressing a question: How the expression of key lncRNAs is altered in the NAc during the formation of morphine addiction memory? To answer these two questions, the mice were trained by using the conditioned place preference (CPP) paradigm. Then, the aberrant expression of lncRNAs was identified in the NAc tissue of the mice by RNA-sequencing.
2023-08-26 | GSE241259 | GEO
Project description:Morphine addiction-NAc_RNA sequencing
| PRJNA823944 | ENA
Project description:Methamphetamine (Meth) seeking progressively increases after withdrawal (incubation of Meth craving), but the transcriptional mechanisms that contribute to this incubation are unknown. Here we used RNA-sequencing to analyze transcriptional profiles associated with incubation of Meth craving in central amygdala (CeA) and orbitofrontal cortex (OFC), two brain areas previously implicated in relapse to drug seeking. We trained rats to self-administer either saline (control condition) or Meth (10 days; 9 h/day, 0.1 mg/kg/infusion). Next, we collected brain tissue from CeA and OFC on withdrawal day 2 (when Meth seeking is low and non-incubated) and on day 35 (when Meth seeking is high and incubated), for subsequent RNA-sequencing. In CeA, we identified 10-fold more differentially expressed genes (DEGs) on withdrawal day 35 than day 2. These genes were enriched for several biological processes, including protein ubiquitination and histone methylation. In OFC, we identified many fewer expression changes than in CeA. Interestingly, there were more DEGs on withdrawal day 2 than on day 35. Several genes in OFC showed opposing expression changes on withdrawal day 2 (increase) when compared to withdrawal day 35 (decrease), which was further validated by qPCR. Our analyses highlight the CeA as a key region of transcriptional regulation associated with incubation of Meth seeking. In contrast, transcriptional regulation in OFC may contributes to Meth seeking during early withdrawal. Overall, these findings provide a unique resource of gene expression data for future studies examining transcriptional mechanisms in CeA that mediate Meth seeking after prolonged withdrawal.
2018-12-26 | GSE111243 | GEO
Project description:Using an oral self-administration paradigm, we have seen morphine increase neural activity in the Paraventricular Nucleus of the Thalamus (PVT). Morphine binds primarily to Mu Opioid Receptors (MORs), which are highly expressed in the PVT. Translating Ribosome Affinity Purification (TRAP)-Sequencing was conducted on PVT neurons that express MORs
2022-10-04 | GSE214560 | GEO
Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
2018-04-16 | E-MTAB-5546 | biostudies-arrayexpress
Project description:Opioid analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit long term use. In the current study using a chronic morphine-murine model a longitudinal approach was undertaken to investigate the role of morphine modulation of gut microbiome as a mechanism contributing to the negative consequences associated with opioids use. The results revealed a significant shift in the gut microbiome and metabolome within 24 hours following morphine treatment when compared to placebo. Morphine induced gut microbial dysbiosis exhibited distinct characteristic signatures profiles including significant increase in communities associated with pathogenic function, decrease in communities associated with stress tolerance. Collectively, these results reveal opioids-induced distinct alteration of gut microbiome, may contribute to opioids-induced pathogenesis. Therapeutics directed at these targets may prolong the efficacy long term opioid use with fewer side effects.
2018-04-16 | E-MTAB-5550 | biostudies-arrayexpress