Mus musculus
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ABSTRACT:
PROVIDER: PRJNA263916 | ENA |
REPOSITORIES: ENA
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Project description:Morphine is used to sedate critically ill infants to treat painful or stressful conditions associated with intensive care. Whether neonatal morphine exposure affects microRNA (miR) expression and thereby alters mRNA regulation is unknown. We tested the hypothesis that repeated morphine treatment in stress-exposed neonatal mice alters hippocampal mRNA and miR gene expression. C57BL/6 male mice were treated from postnatal day (P) 5 to P9 with morphine at 2 or 5 mg/kg ip bid (MS5) and then exposed to stress consisting of hypoxia (100% N2 1 min and 100% O2 5 min) followed by 2h maternal separation. Control mice were untreated and dam-reared. mRNA and microRNA expression profiling was performed on hippocampal tissues at P9. Overall, MS2 and MS5 morphine treatment altered expression of a total of 150 mRNAs (>1.5 fold change, P<0.05; 36 up, 114 down), and MS5 affected 63 mRNAs. The most upregulated mRNAs were fidgetin, arginine vasopressin, and resistin-like alpha, and the most down-regulated were defensin beta 11, aquaporin 1, calmodulin-like 4, chloride intracellular channel 6, and claudin 2. Gene Set Enrichment Analysis revealed that morphine treatment affected pathways related to cell cycle, membrane function, signaling, metabolism, cell death, transcriptional regulation, and immune response. MS5 decreased expression of miR-204-5p, miR-455-3p, miR-448-3p, and miR-574-3p.Nine morphine-responsive mRNAs that are involved in neurodevelopment, neurotransmission, and inflammation are predicted targets of the aforementioned differentially expressed microRNAs These data establish that morphine produces dose-dependent changes in both hippocampal mRNA and miR gene expression in stressed neonatal mice. If permanent, morphine–mediated neuroepigenetic effects may affect long-term hippocampal function, and this provides a mechanism for the neonatal morphine-related impairment of adult learning.
2015-10-05 | GSE62346 | GEO
Project description:We profiled genome-wide gene expression across four brain regions (hippocampus, prefrontal cortex, striatum, and hypothalamus) in male and female C57BL/6NTac mice using a perinatal morphine exposure model of Neonatal Opioid Withdrawal Syndrome (NOWS). Mice received morphine or saline perinatally, then were challenged with LPS or saline in adulthood, yielding four groups (SAL-SAL, SAL-LPS, MOR-SAL, MOR-LPS). NeuN+ neuronal nuclei (~5,000 per sample) were isolated by FACS from PFC, hippocampus, hypothalamus, and striatum and profiled by RNA-seq (Illumina NovaSeq X Plus, paired-end 150 bp). RNA-seq identified differentially expressed genes enriched in immune and metabolic pathways, with the hypothalamus displaying the most pronounced transcriptional response to perinatal morphine exposure.
2026-06-17 | GSE332798 | GEO
Project description:To study the relationship between microRNAs and μ-opioid receptor (MOR) signaling, we examined microRNA expression after chronic morphine or fentanyl treatment in rat primary hippocampal neurons and in mouse hippocampus. Mouse cerebellum region was also tested as a negative control to eliminate microRNA expression changes unrelated to MOR signaling, as the cerebellum is essentially devoid of MOR. We identified a number of microRNAs that altered their expression upon treatment with both morphine and fentanyl in the rat and mouse systems. There were, however, some microRNAs that changed in response to morphine, or fentanyl, but not both. Keywords: Expression profiling
2009-05-04 | GSE14268 | GEO
Project description:To study the relationship between microRNAs and μ-opioid receptor (MOR) signaling, we examined microRNA expression after chronic morphine or fentanyl treatment in rat primary hippocampal neurons and in mouse hippocampus. Mouse cerebellum region was also tested as a negative control to eliminate microRNA expression changes unrelated to MOR signaling, as the cerebellum is essentially devoid of MOR. We identified a number of microRNAs that altered their expression upon treatment with both morphine and fentanyl in the rat and mouse systems. There were, however, some microRNAs that changed in response to morphine, or fentanyl, but not both. Keywords: Expression profiling There are up to three biological replicates (indicated by 1, 2, and 3) of primary hippocampal neurons from new born rats and the cerebellum and hippocampus regions from adult mice treated for three days (control, morphine, and fentanyl). The biological replicates were from experiments performed on different dates. Each biological replicate contained cells or tissues collected from multiple animals so that enough RNA could be extracted for RNA analysis. RNA was labelled with a green dye, mixed with a reference DNA sample labelled with a red dye. The reference DNA contained a number of synthetic DNA oligos with mature microRNA sequences that served to verify microarray hybridization. RNA signals were in ch1, DNA signals ch2.
2010-05-19 | E-GEOD-14268 | biostudies-arrayexpress
Project description:Critically ill preterm infants experience multiple stressors while hospitalized. Morphine is commonly prescribed to ameliorate their pain and stress. We hypothesized that neonatal stress will have a dose-dependent effect on hippocampal gene expression, and these effects will be altered by morphine treatment. Male C57BL/6 mice were exposed to 5 treatment conditions between postnatal day 5 and 9: 1) Control, 2) mild stress + saline, 3) mild stress + morphine, 4) severe stress + saline and 5) severe stress + morphine. Hippocampal RNA was extracted and analyzed using Affymetrix Mouse Gene 1.0 ST Arrays. Single gene analysis and gene set analysis were used to compare groups with validation by qPCR. Stress resulted in enrichment of genes sets related to fear response, oxygen carrying capacity and NMDA receptor synthesis. Morphine downregulated gene sets related to immune function. Stress plus morphine resulted in enrichment of mitochondrial electron transport gene sets, and down-regulation of gene sets related to brain development and growth. We conclude that neonatal stress alone influences hippocampal gene expression, morphine alters a subset of stress-related changes in gene expression and influences other gene sets. Stress plus morphine show interaction effects not present with either stimulus alone. These changes may alter neurodevelopment. Male mice were exposed to 5 treatment conditions between postnatal day (P)5 and P9 (n=3/group), with birth recorded as P1. Litters were culled to n=7 maximum per dam. Groups included: 1) Untreated controls (CC), 2) mild stress + saline (MSS), 3) mild stress + morphine (MSM), 4) severe stress + saline (SSS) and 5) severe stress + morphine (SSM).
2013-08-30 | E-GEOD-50382 | biostudies-arrayexpress
Project description:Transcriptional analysis of neonatal mouse cortex following morphine exposure
| PRJNA935756 | ENA
Project description:miR-7 blockade alters E12.5 mouse cortical mRNA levels
| PRJNA254718 | ENA
Project description:Neonatal morphine is commonly administered in the Neonatal Intensive Care Unit (NICU) to manage pain. However, its long-term effects on neurodevelopment of pain pathways, remain a significant concern. The midbrain is a core region that plays a central role in pain processing and opioid-mediated analgesia. Here, we performed single-cell RNA sequencing to study gene expression in 107,427 midbrain single cells from adolescent mice neonatally exposed to either saline, morphine, or morphine with the probiotic Bifidobacterium infantis (B. infantis). We found broad alterations in transcriptomics within neurons, astrocytes, oligodendrocytes, and microglial cells. Analysis of differentially regulated genes revealed down regulation of HOX genes and upregulation of pathways related to neurotransmitter signaling and pain in adolescence that were neonatally treated with morphine. Interestingly, neonatal probiotic supplementation mitigated these morphine-induced alterations on the transcriptome. This study presents the first single-cell RNA sequencing dataset of the adolescent midbrain following neonatal morphine exposure and probiotic intervention. These findings offer new insights into the neurodevelopmental impact of early opioid exposure and highlight the therapeutic potential of microbiome-targeted interventions.
2025-10-24 | GSE298919 | GEO
Project description:We profiled genome-wide H3K27ac chromatin modifications across four brain regions (hippocampus, prefrontal cortex, striatum, and hypothalamus) in male and female C57BL/6NTac mice using a perinatal morphine exposure model of Neonatal Opioid Withdrawal Syndrome (NOWS). Mice received morphine or saline perinatally, then were challenged with LPS or saline in adulthood, yielding four groups (SAL-SAL, SAL-LPS, MOR-SAL, MOR-LPS). NeuN+ neuronal nuclei (~10,000 per replicate) were isolated by FACS and profiled by MOWChIP-seq (Illumina NovaSeq X Plus, paired-end 150 nt). H3K27ac ChIP-seq identified differentially acetylated enhancers and promoters enriched in immune and metabolic pathways, with the hypothalamus exhibiting the most pronounced chromatin remodeling.
2026-06-17 | GSE332794 | GEO
Project description:Critically ill preterm infants experience multiple stressors while hospitalized. Morphine is commonly prescribed to ameliorate their pain and stress. We hypothesized that neonatal stress will have a dose-dependent effect on hippocampal gene expression, and these effects will be altered by morphine treatment. Male C57BL/6 mice were exposed to 5 treatment conditions between postnatal day 5 and 9: 1) Control, 2) mild stress + saline, 3) mild stress + morphine, 4) severe stress + saline and 5) severe stress + morphine. Hippocampal RNA was extracted and analyzed using Affymetrix Mouse Gene 1.0 ST Arrays. Single gene analysis and gene set analysis were used to compare groups with validation by qPCR. Stress resulted in enrichment of genes sets related to fear response, oxygen carrying capacity and NMDA receptor synthesis. Morphine downregulated gene sets related to immune function. Stress plus morphine resulted in enrichment of mitochondrial electron transport gene sets, and down-regulation of gene sets related to brain development and growth. We conclude that neonatal stress alone influences hippocampal gene expression, morphine alters a subset of stress-related changes in gene expression and influences other gene sets. Stress plus morphine show interaction effects not present with either stimulus alone. These changes may alter neurodevelopment.
2013-08-30 | GSE50382 | GEO