Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA155933 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE35751: Comparative analysis of S100a10-expressing cortical pyramidal cells and whole cortex GSE35758: Comparative analysis of S100a10 and Glt25d2 cortical pyramidal cells GSE35761: Effect of fluoxetine treatment on translational profiles of S100a10 cortical pyramidal cells GSE35763: Effect of fluoxetine treatment on translational profiles of Glt25d2 cortical pyramidal cells GSE35765: Effect of fluoxetine treatment on translational profiles of S100a10 cortical pyramidal cells in p11 KOs Refer to individual Series
2012-05-31 | E-GEOD-35766 | biostudies-arrayexpress
Project description:Effect of fluoxetine treatment on translational profiles of S100a10 cortical pyramidal cells in p11 KOs
| PRJNA155937 | ENA
Project description:Effect of fluoxetine treatment on translational profiles of Glt25d2 cortical pyramidal cells
| PRJNA155935 | ENA
Project description:Comparative analysis of S100a10 and Glt25d2 cortical pyramidal cells
| PRJNA155931 | ENA
Project description:Comparative analysis of S100a10-expressing cortical pyramidal cells and whole cortex
| PRJNA155923 | ENA
Project description:Molecular phenotyping of cell types and neural circuits underlying pathological neuropsychiatric conditions and their responses to therapy provides one avenue for the development of more specific and effective treatments. In this study, we identify a cell population in the cerebral cortex that shows robust and specific molecular adaptations following long-term SSRI treatment. We employed the bacTRAP strategy, which uses BAC transgenic mice expressing EGFP-tagged ribosomal protein L10a in specific cell populations, to affinity purify polysome-bound mRNAs from S100a10-expressing corticostriatal projection neurons. We show that the S100a10 cells are a unique population of cortical cells that are strongly and specifically responsive to chronic SSRI administration and that this response requires p11 (the protein product of S100a10). Our data demonstrate that the beneficial actions of antidepressant therapy can be mediated by a single cell type that is positioned to normalize activity between cortical and subcortical sites, and suggest that development of drugs that specifically target the activity of these cells may result in improved therapies to treat depression. S100a10 bacTRAP mice crossed to constitutive p11 KO mice (S100a10 bacTRAP/p11 KO) were administered either fluoxetine (FLX) or vehicle (VEH) in their drinking water for 15-18 days. Three independent TRAP replicates from the cortex of each group were then collected. Total RNA from the immunoprecipitates was amplified and hybridized. Data were normalized with the GCRMA algorithm and replicates were averaged across conditions. We recommend filtering data to remove probe sets with normalized expression values less than 50 in at least one condition. Because the S100a10 BAC labels some non-neuronal cells, we recommend only probe sets listed in Table S1 of the accompanying paper be included in the analysis.
2012-05-31 | E-GEOD-35765 | biostudies-arrayexpress
Project description:Molecular phenotyping of cell types and neural circuits underlying pathological neuropsychiatric conditions and their responses to therapy provides one avenue for the development of more specific and effective treatments. In this study, we identify a cell population in the cerebral cortex that shows robust and specific molecular adaptations following long-term SSRI treatment. We employed the bacTRAP strategy, which uses BAC transgenic mice expressing EGFP-tagged ribosomal protein L10a in specific cell populations, to affinity purify polysome-bound mRNAs from S100a10-expressing corticostriatal projection neurons. We show that the S100a10 cells are a unique population of cortical cells that are strongly and specifically responsive to chronic SSRI administration and that this response requires p11 (the protein product of S100a10). Our data demonstrate that the beneficial actions of antidepressant therapy can be mediated by a single cell type that is positioned to normalize activity between cortical and subcortical sites, and suggest that development of drugs that specifically target the activity of these cells may result in improved therapies to treat depression. S100a10 bacTRAP mice were administered either fluoxetine (FLX) or vehicle (VEH) in their drinking water for 15-18 days. Three independent TRAP replicates from the cortex of each group were then collected. Total RNA from the immunoprecipitates was amplified and hybridized. Data were normalized with the GCRMA algorithm and replicates were averaged across conditions. We recommend filtering data to remove probe sets with normalized expression values less than 50 in at least one condition. Because the S100a10 BAC labels some non-neuronal cells, we recommend only probe sets listed in Table S1 of the accompanying paper be included in the analysis.
2012-05-31 | E-GEOD-35761 | biostudies-arrayexpress
Project description:Effect of chronic fluoxetine treatment on hippocampal gene expression
| PRJNA98715 | ENA
Project description:Molecular phenotyping of cell types and neural circuits underlying pathological neuropsychiatric conditions and their responses to therapy provides one avenue for the development of more specific and effective treatments. In this study, we identify a cell population in the cerebral cortex that shows robust and specific molecular adaptations following long-term SSRI treatment. We employed the bacTRAP strategy, which uses BAC transgenic mice expressing EGFP-tagged ribosomal protein L10a in specific cell populations, to affinity purify polysome-bound mRNAs from S100a10-expressing corticostriatal projection neurons. We show that the S100a10 cells are a unique population of cortical cells that are strongly and specifically responsive to chronic SSRI administration and that this response requires p11 (the protein product of S100a10). Our data demonstrate that the beneficial actions of antidepressant therapy can be mediated by a single cell type that is positioned to normalize activity between cortical and subcortical sites, and suggest that development of drugs that specifically target the activity of these cells may result in improved therapies to treat depression. Glt25d2 bacTRAP mice were administered either fluoxetine (FLX) or vehicle (VEH) in their drinking water for 15-18 days. Three independent TRAP replicates from cortex of each group were then collected. Total RNA from the immunoprecipitates was amplified and hybridized. Data were normalized with the GCRMA algorithm and replicates were averaged across conditions. We recommend filtering data to remove probe sets with normalized expression values less than 50 in at least one condition. Because the S100a10 BAC labels some non-neuronal cells, we recommend only probe sets listed in Table S1 of the accompanying paper be included in the analysis.
2012-05-31 | E-GEOD-35763 | biostudies-arrayexpress
Project description:Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed antidepressant drugs in pregnant women. Given that SSRIs can cross the placental and blood-brain barriers, these drugs potentially affect serotonergic neurotransmission and neurodevelopment in the fetus. Although no gross SSRI-related teratogenic effect has been reported, infants born following prenatal exposure to SSRIs have a higher risk for various behavioral abnormalities. Therefore, we examined the effects of prenatal fluoxetine, the most commonly prescribed SSRI, on social and cognitive behavior in mice. Intriguingly, chronic in utero fluoxetine treatment impaired working memory and social novelty recognition in adult males with augmented spontaneous inhibitory synaptic transmission onto the layer 5 pyramidal neurons in the medial prefrontal cortex (mPFC). Moreover, fast-spiking interneurons in the layer 5 mPFC exhibited enhanced basal intrinsic excitability, augmented serotonin-induced neuronal excitability, and increased inhibitory synaptic transmission onto the layer 5 pyramidal neurons due to augmented 5-HT2A receptor (5-HT2AR) signaling. More importantly, the observed behavioral deficits of in utero fluoxetine-treated mice could be reversed by acute systemic application of 5-HT2AR antagonist. Taken together, our findings support the notion that alterations in serotonin-mediated inhibitory neuronal modulation result in reduced cortical network activities and cognitive impairment following prenatal exposure to SSRIs.
2018-03-07 | GSE111491 | GEO