Mus musculus
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-6511
PROVIDER: PRJNA104251 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series:; GSE6467: Twelve weeks expression data of the antipsychotics Clozapine and Haloperidol in the mouse brain (Affymetrix, GCRMA). GSE6511: Four weeks expression data of the antipsychotics Clozapine and Haloperidol in the mouse brain (Affymetrix, GCRMA). Experiment Overall Design: Refer to individual Series
2008-06-14 | E-GEOD-6512 | biostudies-arrayexpress
Project description:Twelve weeks expression data of the antipsychotics Clozapine and Haloperidol in the mouse brain (Affymetrix, GCRMA).
| PRJNA104237 | ENA
Project description:Atypical antipsychotic Clozapine has a superior antipsychotic and antimanic effects compared to other antisphicotics. Its widespread use was limited by the side effects of agranulocytosis, cardiomyopathy and metabolic anomalies such as weight gain, and diabetes. Very little is known about mechanisms by which Clozapine works. The aim of this experiment is to compare the chronic gene expression profile (i.e four weeks) of the atypical antipsychotic Clozapine to the typical antipsychotic drug Haloperidol using gene expression Microarray in order to understand the intercellular mechanism behind the therapeutic and the toxic effects of Clozapine. Experiment Overall Design: The study was designed to compare the chronic therapeutic and toxic expression profile of Clozapine to Haloperidol in the mouse brain. All experiments were performed in male C57BL mice at four weeks of age (Biological services, University Collage London). Several theoretical and practical considerations influenced the final experimental design. To avoid the effect of injections on genesâ expression and to simulate the clinical scenario in human, both drugs were applied to the animalsâ drinking water using the maximum human therapeutic dose (i.e.1.6mg/kg/day for Haloperidol and 12mg/kg/day for Clozapine).Thirty animals were divided equally between three treatment groups and received either Haloperidol (10 animals), Clozapine (10 animals) or no treatment (10 animals) for 4 weeks. After four weeks,the plasma drug level for both drugs was assesed by Tandem mass Spectrometry LC- MS/MS. The total RNA from the right forebrains of nine selected animals (three from each treatment group) were extracted and hybridized to the Affymetrix U74Av2. In all the Microarray experiments we have avoided pooling and each RNA sample was an independent biological replicate. The total numbers of used arrays were 9 Affymetrix U74Av2.
2009-04-30 | E-GEOD-6511 | biostudies-arrayexpress
Project description:Atypical antipsychotic Clozapine has a superior antipsychotic and antimanic effects compared to other antisphicotics. Its widespread use was limited by the side effects of agranulocytosis, cardiomyopathy and metabolic anomalies such as weight gain, and diabetes. Very little is known about mechanisms by which Clozapine works. The aim of this experiment is to compare the chronic gene expression profile of the atypical antipsychotic Clozapine to the typical antipsychotic drug Haloperidol using gene expression Microarray in order to understand the intercellular mechanism behind the therapeutic and the toxic effects of Clozapine. Experiment Overall Design: The study was designed to compare the chronic therapeutic and toxic expression profile of Clozapine to Haloperidol in the mouse brain. All experiments were performed in male C57BL mice at four weeks of age (Biological services, University Collage London). Several theoretical and practical considerations influenced the final experimental design. To avoid the effect of injections on genes expression and to simulate the clinical scenario in human, both drugs were applied to the animals drinking water using the maximum human therapeutic dose (i.e. 1.6mg/kg/day for Haloperidol and 12mg/kg/day for Clozapine). Thirty animals were divided equally between three treatment groups and received either Haloperidol (10 animals), Clozapine (10 animals) or no treatment (10 animals) for 12 weeks. After twelve weeks, the total RNA from the right forebrains were extracted and hybridized to the Affymetrix MOE430A array. In all the Microarray experiments we have avoided pooling and each RNA sample was an independent biological replicate. The total numbers of used arrays were 30 Affymetrix MOE430A arrays.
2009-02-07 | E-GEOD-6467 | biostudies-arrayexpress
Project description:Atypical antipsychotic Clozapine has a superior antipsychotic and antimanic effects compared to other antisphicotics. Its widespread use was limited by the side effects of agranulocytosis, cardiomyopathy and metabolic anomalies such as weight gain, and diabetes. Very little is known about mechanisms by which Clozapine works. The aim of this experiment is to compare the chronic gene expression profile (i.e four weeks) of the atypical antipsychotic Clozapine to the typical antipsychotic drug Haloperidol using gene expression Microarray in order to understand the intercellular mechanism behind the therapeutic and the toxic effects of Clozapine. Keywords: drug response
2006-12-13 | GSE6511 | GEO
Project description:Transcription profiling of mouse brain from animals treated for 4 weeks with the antipsychotics Clozapine and Haloperidol
2015-10-13 | E-GEOD-6511 | ExpressionAtlas
Project description:Clozapine and Haloperidol effect on the mouse brain
| PRJNA98595 | ENA
Project description:Although antipsychotics are routinely used in the treatment of schizophrenia for last decades, their precise mechanism of action is still unclear. In this study we investigated changes in PC12 cells’ proteome under the influence of clozapine, risperidone and haloperidol to identify protein pathways regulated by the antipsychotics. Analysis of the protein profiles in two time points: after 12 and 24 h of incubation with drugs revealed significant alterations in 510 proteins. Further canonical pathway analysis determined signal transduction pathways and biological processes regulatednby drug treatment. Interestingly, all tested drugs have caused changes in PC12 proteome which correspond to inhibition of cytokines: tumor necrosis factor (TNF) and transforming growth factor beta 1 (TGF-β1), what can be linked to the immunological and viral hypothesis of schizophrenia. We found, that the 12-hour incubation with clozapine caused up-regulation of protein kinase A signalling and translation machinery. After 24 h of treatment with clozapine, the inhibition of the actin cytoskeleton signalling and Rho proteins signalling was revealed. Obtained results suggests that mammalian target of rapamycin complex 1 (mTORC1) and 2 (mTORC2) play a central role in the signal transduction of clozapine.
2021-09-08 | PXD014422 | Pride
Project description:To identify the molecular mechanisms that may initiate therapeutic effects, whole-genome expression profiling (Illumina Mouse WG-6 microarrays) of drug-induced alterations in the mouse brain was undertaken, with a focus on the time-course (1, 2, 4 and 8h) of gene expression changes produced by eighteen major psychotropic drugs: antidepressants, antipsychotics, anxiolytics, psychostimulants and opioids. The resulting database is freely accessible at www.genes2mind.org. Bioinformatics approaches led to the identification of three main drug-responsive genomic networks and indicated neurobiological pathways that mediate the alterations in transcription. Each tested psychotropic drug was characterized by a unique gene network expression profile related to its neuropharmacological properties. Functional links that connect expression of the networks to the development of neuronal adaptations (MAPK signaling pathway), control of brain metabolism (adipocytokine pathway), and organization of cell projections (mTOR pathway) were found. The additional data-sets are available at GEOX1 and GEOX2. The microarray experiment was performed to analyze time-course of drug-induced transcriptional response in C57BL/6J mouse striatum. Three antidepressants (bupropion 20 mg/kg, tranylcypromine 20 mg/kg, mianserin 20 mg/kg, i.p.), three anxiolytics (diazepam 5 mg/kg, buspirone 10 mg/kg, hydroxyzine 10 mg/kg, i.p.), and three antipsychotics (clozapine 3 mg/kg, risperidone 0.5 mg/kg, haloperidol 1 mg/kg) were selected for the comparison. Drug doses were previously reported as effective in mice and further tested in our laboratory. To analyze dynamics of early, intermediate and relatively late changes of mRNA abundance the experiment was performed in four time points (1, 2, 4 and 8h after drug administration). To exclude influence of drug injection and circadian rhythm on gene expression profile, control groups of saline or tween (1% Tween 80) treated and naïve animals were prepared for each time point. Design of the experiment assumed pooling of two animals per each array and using of three independent arrays per group. To provide appropriate balance in the whole dataset groups were equally divided between the array hybridization batches.
2013-07-18 | E-GEOD-48954 | biostudies-arrayexpress
Project description:This work reveals the effect of antipsychotics on DNA methylation using the cell model. After the treatment of antipsychotics, haloperidol and risperidone, DNA methylation profiles obtained by Illumina HumanMethylation450 beadchip were examined.
2021-11-02 | GSE185973 | GEO