Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analgesia of naloxone and morphine in wild-type and NY1DD sickle cell mice using BMAP cDNA microarrays

ABSTRACT: Sickle cell disease is the most common genetic disorder in African-Americans. The opioid analgesic, morphine, has long been the treatment for the severe pain associated with this disease. Here we reveal that the opioid antagonist, naloxone, possesses potent analgesic activity in two strains of sickle cell mice (NY1DD and hBERK1) and not in their respective controls (ICR-CD1 and C57BL/6J) when administered by three parenteral routes. In the NY1DD sickle mice, naloxone (i.c.v.) possessed ~300-fold greater potency than morphine (i.c.v.). Other opioid antagonists (naltrexone, norbinaltorphimine, naltrindole) were substantially less effective in producing analgesia. Naloxone and morphine were synergistic in NY1DD mice, suggesting that analgesia was mediated via different receptor systems. Since microarray analysis suggested naloxone-induced down-regulation of the CCR5 chemokine receptor in NY1DD mice but not in control mice, the role of its endogenous ligand, CCL5 (RANTES), was investigated. Keywords: Comparison of drug induced gene expression

ORGANISM(S): Mus musculus

PROVIDER: GSE6479 | GEO | 2007/12/20

SECONDARY ACCESSION(S): PRJNA98721

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Analgesia of naloxone in wild-type and NY1DD transgenic mouse model of sickle cell anemia using BMAP cDNA microarrays

Project description:Sickle cell disease is the most common genetic disorder in African-Americans. The opioid analgesic, morphine, has long been the treatment for the severe pain associated with this disease. Here we reveal that the opioid antagonist, naloxone, possesses potent analgesic activity in two strains of sickle cell mice (NY1DD and hBERK1) and not in their respective controls (ICR-CD1 and C57BL/6J) when administered by three parenteral routes. In the NY1DD sickle mice, naloxone (i.c.v.) possessed ~300-fold greater potency than morphine (i.c.v.). Other opioid antagonists (naltrexone, norbinaltorphimine, naltrindole) were substantially less effective in producing analgesia. Naloxone and morphine were synergistic in NY1DD mice, suggesting that analgesia was mediated via different receptor systems. Since microarray analysis suggested naloxone-induced down-regulation of the CCR5 chemokine receptor in NY1DD mice but not in control mice, the role of its endogenous ligand, CCL5 (RANTES), was investigated. Keywords: Comparison of drug induced gene expression

2007-03-14 | GSE6578 | GEO

Naloxone influences NSCs proliferation and differentiation

Project description:Naloxone is an opioid-receptor antagonist used to reverse the effects of opioid.In our study, we treated NSCs (neural stem cells) with naloxone and damgo (a selective μopioid receptor agonist), and examined their effects on NSCs proliferation and differentiation.Naloxone was found to promote NSCs proliferation and neural differentiation, while the effects of damgo was very week. The results suggested that naloxone may work indepedent of opioid receptors. To investigate the underlying mechanisms, RNA-seq was conducted. For proliferation analysis,p8 NSCs were cultured with or without naloxone or damgo for 3 days. For differentiation analysis,p8 NSCs was induced to differentiate with or without naloxone or damgo, samples on D2,4,8 were collected and analyzed.

2020-03-04 | GSE106376 | GEO

Effects of naloxone on NSC proliferation and differentiation

2020-10-27 | GSE106263 | GEO

DNA methylation maps of mouse NSCs treated with naloxone

Project description:In our study,we examined the effects of naloxone (an opioid receptor antagonist) on NSCs (neural stem cells) proliferation and differenntiation. Briefly, we treated NSCs with naloxone in the proliferation and differentiation system. Naloxone was shown to acclerate NSCs proliferation and increase neural differentiation.To investigate how DNA methylation is affected upon naloxone treatment, cells cultured 3 days with naloxone and cells differentiated with naloxone at D2 were collected, genomic DNA was extracted and subjected to RRBS analysis.

2020-03-04 | GSE107525 | GEO

Mus musculus

Project description:Analgesia of naloxone and morphine in wild-type and NY1DD sickle cell mice using BMAP cDNA microarrays

| PRJNA98721 | ENA

The molecular basis of analgesia in congenital insensitivity to pain associated with loss of Nav1.7 function

Project description:Loss of function mutations in the SCN9a gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain (CIP) and anosmia in otherwise normal humans and mice, suggesting that this channel may be a good analgesic drug target. Surprisingly, potent selective antagonists of Nav1.7 are weak analgesics. We therefore investigated whether Nav1.7 , as well as contributing to electrical signalling may have an additional function. Here we report that Nav1.7 deletion has profound effects on the sensory neuron transcriptome, leading to dysregulation of a number of transcription factors as well as upregulation of enkephalin precursor PENK mRNA and down regulation of CEACAM10 mRNA, a protein involved in noxious thermosensation. PENK mRNA is transcriptionally upregulated in Nav1.7 null mutant female sensory neurons, resulting in increased enkephalin expression in the dorsal horn of the spinal cord. PENK expression is down-regulated by addition of the sodium ionophore monensin, suggesting that sodium may play a role as a second messenger. Application of the opioid antagonist naloxone strongly enhances noxious peripheral input into the spinal cord, and dramatically reduces analgesia in both male and female Nav1.7 null mutant mice, as well as in human Nav1.7 null mutants. These data show that loss of Nav1.7 expression increases opioid drive over the lifetime of mice and humans. They further suggest that Nav1.7 channel blockers alone may not replicate the phenotype of null mutant humans and mice, but should be potentiated with exogenous opioids. RNA was extracted from Dorsal Root Ganglia tissue from Nav1.7 Knock-Out, Nav1.8 KO and Nav1.9 KO mice (n = 3) and hybridised on Affymetrix Mouse Genome 430 2.0 Array (GPL1261)

2014-09-13 | E-GEOD-61373 | biostudies-arrayexpress

Naloxone in Treating Constipation in Patients Who Are Receiving Opioids for Chronic Pain

Project description:RATIONALE: Naloxone may be effective in treating constipation that may be caused by opioid pain medications such as morphine. PURPOSE: Phase III trial to determine the effectiveness of naloxone in relieving constiption in patients who are receiving opioids for chronic pain.

| 2006458 | ecrin-mdr-crc

Suppression of RGSz1 function optimizes the actions of opioid analgesics by mechanisms that involve the Wnt/β-catenin pathway

Project description:Regulator of G protein signaling z1 (RGSz1), a member of the RGS family of proteins, is present in several networks expressing mu opioid receptors (MOPR). By using genetic mouse models for global or brain region-targeted manipulations of RGSz1 expression, we demonstrate that the suppression of RGSz1 function increases the analgesic efficacy of MOPR agonists in male and female mice and delays the development of morphine tolerance while decreasing the sensitivity to rewarding and locomotor activating effects. Using biochemical assays and next-generation RNA sequencing, we identified a key role of RGSz1 in the periaqueductal gray (PAG) in morphine tolerance. Chronic morphine administration promotes RGSz1 activity in the PAG, which in turn modulates transcription mediated by the Wnt/β-catenin signaling pathway to promote analgesic tolerance to morphine. Conversely, the suppression of RGSz1 function stabilizes Axin2-Gaz complexes near the membrane and promotes β-catenin activation, thereby delaying the development of analgesic tolerance. These data show that the regulation of RGS complexes, particularly those involving RGSz1-Gaz, represents a promising target for optimizing the analgesic actions of opioids without increasing the risk of dependence or addiction.

2018-01-12 | GSE109165 | GEO

The molecular basis of analgesia in congenital insensitivity to pain associated with loss of Nav1.7 function

2014-09-13 | GSE61373 | GEO

Morphine-responsive neurons that regulate mechanical antinociception

Project description:Opioids are widely used, effective analgesics to manage severe acute and chronic pain, although they have recently come under scrutiny because of epidemic levels of abuse. While these compounds act on numerous central and peripheral pain pathways, the neuroanatomical substrate for opioid analgesia is not fully understood. By means of single-cell transcriptomics and manipulation of morphine-responsive neurons, have identified an ensemble of neurons in the rostral ventromedial medulla (RVM) that regulates mechanical nociception in mice. Among these, forced activation or silencing of excitatory RVMBDNF projection neurons mimicked or completely reversed morphine-induced mechanical antinociception, respectively, via a brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)-dependent mechanism and activation of inhibitory spinal galanin-positive neurons. Our results reveal a specific RVM-spinal circuit that scales mechanical nociception whose function confers the antinociceptive properties of morphine.

2024-08-30 | GSE253816 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data