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Transcriptomic profiling of mouse amygdala during opioid dependence and withdrawal by single-cell RNA sequencing

ABSTRACT: The development of substance use disorder (SUD) is a complex process involving multiple neurocircuitries and brain regions. The amygdala is a region that mediates the withdrawal effect as well as anxiety and depression-like behaviors. However, the transcriptional changes in each cell type during SUD is largely unknown. Here we performed single-cell RNA sequencing and classified all cell types in the mouse amygdala under opioid dependence and withdrawal states. Our data revealed distinct changes in key biological processes, such as immune response, inflammation, synaptic transmission, and mitochondrial respiration in different cell populations. Dramatic differences were unraveled in the transcriptional profiles between dependence and withdrawal states. This report is the first single-cell RNA sequencing dataset from the amygdala under opioid dependence and withdrawal conditions, providing unique insights in understanding brain alterations during SUD, especially at the molecular and cellular levels.

ORGANISM(S): Mus musculus

PROVIDER: GSE207128 | GEO | 2023/11/08

REPOSITORIES: GEO

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Project description:Opioids analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit their use. It has been recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. Further study indicated distinct alterations in the gut microbiome and metabolome following morphine treatment, contributing to the negative consequences associated with opioid use. However, it is unclear how opioids modulate gut homeostasis in the context of a hospital acquired bacterial infection. In the current study, a mouse model of C. rodentium infection was used to investigate the role of morphine in the modulation of gut homeostasis in the context of a hospital acquired bacterial infection. Citrobacter rodentium is a natural mouse pathogen that models intestinal infection by enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) and causes attaching and effacing lesions and colonic hyperplasia. Morphine treatment resulted in 1) the promotion of C. rodentium systemic dissemination, 2) increase in virulence factors expression with C. rodentium colonization in intestinal contents, 3) altered gut microbiome, 4) damaged integrity of gut epithelial barrier function, 5) inhibition of C. rodentium-induced increase in goblet cells, and 6) dysregulated IL-17A immune response. This is the first study to demonstrate that morphine promotes pathogen dissemination in the context of intestinal C. rodentium infection, indicating morphine modulates virulence factor-mediated adhesion of pathogenic bacteria and induces disruption of mucosal host defense during C. rodentium intestinal infection in mice. This study demonstrates and further validates a positive correlation between opioid drug use/abuse and increased risk of infections, suggesting over-prescription of opioids may increase the risk in the emergence of pathogenic strains and should be used cautiously. Therapeutics directed at maintaining gut homeostasis during opioid use may reduce the comorbidities associated with opioid use for pain management.

Dataset Information

Transcriptomic profiling of mouse amygdala during opioid dependence and withdrawal by single-cell RNA sequencing

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