Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA110009 | ENA |
REPOSITORIES: ENA
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Project description:Soman (O-Pinacolyl methylphosphonofluoridate) is a potent neurotoxicant. Acute exposure to soman causes profound inhibition of the critical enzyme acetylcholinesterase, resulting in excessive levels of the neurotransmitter acetylcholine. Excessive acetylcholine levels cause convulsions, seizures, and respiratory distress. The initial cholinergic crisis can be overcome by rapid anti-cholinergic therapeutic intervention, resulting in increased survival. However, conventional treatments do not protect the brain from seizure-related damage, and thus neurodegeneration of soman-sensitive areas of the brain is a potential post-exposure outcome. We performed gene expression profiling of rat hippocampus following soman exposure to gain greater insight into the molecular pathogenesis of soman-induced neurodegeneration. Keywords: Time-course; toxicant exposure
2009-03-13 | GSE13428 | GEO
Project description:Soman (O-Pinacolyl methylphosphonofluoridate) is a potent neurotoxicant. Acute exposure to soman causes profound inhibition of the critical enzyme acetylcholinesterase, resulting in excessive levels of the neurotransmitter acetylcholine. Excessive acetylcholine levels cause convulsions, seizures, and respiratory distress. The initial cholinergic crisis can be overcome by rapid anti-cholinergic therapeutic intervention, resulting in increased survival. However, conventional treatments do not protect the brain from seizure-related damage, and thus neurodegeneration of soman-sensitive areas of the brain is a potential post-exposure outcome. We performed gene expression profiling of rat hippocampus following soman exposure to gain greater insight into the molecular pathogenesis of soman-induced neurodegeneration. Experiment Overall Design: Male Sprague-Dawley rats were pretreated with the oxime HI-6 (l-(((4-aminocarbonyl)pyridinio)methoxyl)methyI)-2-((hydroxyimino)methyl)-pyridinium dichloride; 125 mg/kg, ip) 30 min prior to challenge with soman (180 μg/kg, sc; diluted with 0.9% sodium chloride). One minute after soman challenge, animals were treated with atropine methyl nitrate (2.0 mg/kg, im). Vehicle control animals (n=4; 2 euthanized at 1h, 1 euthanized at 12h, and 1 euthanized at 24h) received an equivalent volume of vehicle (0.9% sodium chloride), HI-6 and atropine. Naïve animals (n=3) were also included in the study and received no treatments. Hippocampal tissue was harvested 1, 3, 6, 12, 24, 48, 72, 96, and 168h after soman exposure. A sample size of n=3 was used for all time points except 3h (n=6) and 72h (n=4). RNA was extracted from the hippocampal tissue and used to generate oligonucleotide microarray probes for gene expression profiling using Affymetrix Rat 230 2.0 microarrays.
2009-03-21 | E-GEOD-13428 | biostudies-arrayexpress
Project description:Gene Expression Changes in the Rat Nasal Epithelium Following Formaldehyde Exposure
| PRJNA99247 | ENA
Project description:Gene expression profiles in the cerebellum and hippocampus following exposure to neurotoxicant Aroclor 1254
| PRJNA110551 | ENA
Project description:Expression data from neonatal rat ovaries following LPS exposure
| PRJNA200339 | ENA
Project description:DNA methylation changes in rat sperm following exposure to THC
| PRJNA633085 | ENA
Project description:Intracranial self-stimulation regulates gene expression in rat hippocampus
| PRJNA183164 | ENA
Project description:A series of two color gene expression profiles obtained using Agilent 44K expression microarrays was used to examine sex-dependent and growth hormone-dependent differences in gene expression in rat liver. This series is comprised of pools of RNA prepared from untreated male and female rat liver, hypophysectomized (‘Hypox’) male and female rat liver, and from livers of Hypox male rats treated with either a single injection of growth hormone and then killed 30, 60, or 90 min later, or from livers of Hypox male rats treated with two growth hormone injections spaced 3 or 4 hr apart and killed 30 min after the second injection. The pools were paired to generate the following 6 direct microarray comparisons: 1) untreated male liver vs. untreated female liver; 2) Hypox male liver vs. untreated male liver; 3) Hypox female liver vs. untreated female liver; 4) Hypox male liver vs. Hypox female liver; 5) Hypox male liver + 1 growth hormone injection vs. Hypox male liver; and 6) Hypox male liver + 2 growth hormone injections vs. Hypox male liver. A comparison of untreated male liver and untreated female liver liver gene expression profiles showed that of the genes that showed significant expression differences in at least one of the 6 data sets, 25% were sex-specific. Moreover, sex specificity was lost for 88% of the male-specific genes and 94% of the female-specific genes following hypophysectomy. 25-31% of the sex-specific genes whose expression is altered by hypophysectomy responded to short-term growth hormone treatment in hypox male liver. 18-19% of the sex-specific genes whose expression decreased following hypophysectomy were up-regulated after either one or two growth hormone injections. Finally, growth hormone suppressed 24-36% of the sex-specific genes whose expression was up-regulated following hypophysectomy, indicating that growth hormone acts via both positive and negative regulatory mechanisms to establish and maintain the sex specificity of liver gene expression. For full details, see V. Wauthier and D.J. Waxman, Molecular Endocrinology (2008)
2008-05-24 | GSE11529 | GEO
Project description:Transcriptomic Analysis of Rat Brain Following Exposure to the Organophosphonate Anticholinesterase Sarin
| PRJNA139241 | ENA