Mus musculus
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ABSTRACT:
PROVIDER: PRJNA142873 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE29138: The mRNA expression patterns in macaque brains from prenatal to neonatal GSE29139: Identification of response genes upon neuronal activation in mouse cortical neurons Refer to individual Series
2012-02-02 | E-GEOD-29140 | biostudies-arrayexpress
Project description:We search for developmental changes specific to humans by examining gene expression profiles in the human, chimpanzee and rhesus macaque prefrontal and cerebellar cortex. In both brain regions, developmental patterns were more evolved in humans than in chimpanzees. The major human specific genes in prefrontal cortex was enriched in neuronal functions and regulated by several transcription factors, which were previously implicated in regulation of neuronal functions. To confirm neuronal function of the human prefrontal cortex specific genes, we identifed response genes upon neuronal activation in mouse cortical neurons. Our results show that human specific genes are enriched in the response genes upon neuronal activation, implying the function of human prefrontal cortex specific genes in synaptic development. The cortical neurons from E15 mouse were isolated and cultured. We then exposed neurons to bicuculline (Bic), or potassium chloride (KCl), or without treatment. The cultured neurons under each group were hybridized to Agilent whole mouse genome oligo microarray (4x44k).
2012-02-02 | E-GEOD-29139 | biostudies-arrayexpress
Project description:We search for developmental changes specific to humans by examining gene expression profiles in the human, chimpanzee and rhesus macaque prefrontal and cerebellar cortex. In both brain regions, developmental patterns were more evolved in humans than in chimpanzees. The major human specific genes in prefrontal cortex was enriched in neuronal functions and regulated by several transcription factors, which were previously implicated in regulation of neuronal functions. To confirm neuronal function of the human prefrontal cortex specific genes, we identifed response genes upon neuronal activation in mouse cortical neurons. Our results show that human specific genes are enriched in the response genes upon neuronal activation, implying the function of human prefrontal cortex specific genes in synaptic development.
2012-02-02 | GSE29139 | GEO
Project description:Activation of neurons is one of the fundamental events for the functioning of nervous system. Neuronal activation relays information to next neurons. On the other hand, the activated neurons themselves are also influenced by neuronal activation. Depending on the type and condition of neuronal activation, these activated neurons change their gene expressions, thereby being able to process information more or less efficiently. We applied the microarray technology to identify hither-to-uncharacterized as activity-dependent genes. Especially, we screened the transcription factors, because early changes in the transcription factors should result in alterations of gene expression profiles and subsequent neuronal properties. Experiment Overall Design: Rat primary cortical neurons with or without KCl treatment were selected for RNA extraction and hybridization on Affymetrix microarrays. To identify the genes whose expression was induced by depolarization, we first compared gene expression profiles in control vs. 4 hr after KCl (25 mM) treated cortical neurons using Affymetrix Genechips specified for neurobiology. All four hybridizations were analyzed for correlation accuracy between the replicates of the same treatments .Control replicates (control 1, 2) KCl-treated replicates (KCl 1, 2)
2008-06-13 | E-GEOD-4472 | biostudies-arrayexpress
Project description:KCl depolarization-regulated genes in mouse cortical neurons
| PRJNA109193 | ENA
Project description:For identification of transcripts enriched in neurites of primary cortical neurons, the cells were plated on a microporous membrane for isolation of neurites and soma. Extracted RNA was used for preparation of mRNA-seq, total RNA-seq or smRNA-seq libraries and Illumina sequencing. For neuronal zipcode identification protocol (N-zip) in mouse cortical neurons, we combined a massively parallel reporter assay with neurites/soma separation. Neurons, grown on a microporous membrane, were infected with a library of around 5000 oligos tiled across 3'UTRs of selected neurite-enriched transcripts, cloned downstream of GFP coding sequence. RNA was extracted from soma and neurites and reverse transcribed into cDNA. Amplicon libraries of 3'UTR reporters were prepared and subjected to Illumina sequencing. In the second round of N-zip, a library containing selected reporters from the first N-zip and their mutagenized versions (around 6000 oligos) were used. In the following rounds, N-zip was combined with knockdown of selected genes.
2022-12-02 | E-MTAB-10902 | biostudies-arrayexpress
Project description:Primary cortical neurons were isolated from E15 mice and after 5 days in vitro were untreated or treated for 24 h with mesenchymal stem cell conditioned medium and then untreated or treated for a further 24 h with NMDA. Neuron gene expression was profiled and compared between the four different conditions (neurons, neurons+MSC cm, neurons+NMDA, neurons+MSC cm+NMDA) to investigate the molecular mechanisms of MSC neuroprotection. Mesenchymal stem cells (MSC) promote functional recovery in experimental models of central nervous system (CNS) pathology and are currently being tested in clinical trials for stroke, multiple sclerosis and CNS injury. Their beneficial effects are attributed to activation of endogenous CNS repair processes and immune regulation but their mechanisms of action are poorly understood. Here we investigated the neuroprotective effects of MSC in simplified MSC-neuron co-culture systems and in mice using models of glutamate excitotoxicity. MSC protected primary cortical neurons against glutamate (NMDA) receptor-induced death and conditioned medium from MSC (MSC cm), but not control NIH3T3 cells, was sufficient for this effect. MSC cm neuroprotection in mouse cortical neurons was reduced by neutralizing antibodies to bFGF and associated with altered gene expression in neurons towards an immature phenotype as well as reduced neuronal Grin1, Grin2a and Grin2b mRNA levels in response to NMDA stimulation. Further, MSC cm neuroprotection in rat retinal ganglion cells was associated with absence of glutamate-induced calcium influx. Adoptive transfer of EGFP+MSC in a mouse kainic acid seizure model reduced CA3 neuron damage and hippocampal astrocytosis and resulted in the increased expression of neuronal genes that are upregulated by MSC cm, Bmi1, Ddx4, Ezh1, in the hippocampus. These results show that MSC mediate direct neuroprotection against glutamate excitotoxicity by secreting bFGF, reducing glutamate receptor expression and function and altering neuron gene expression towards an immature pattern, and provide evidence for a link between the therapeutic effects of MSC and the activation of endogenous repair processes following CNS injury. In vitro cultures primary cortical neurons from mice were protected from glutamate excitotoxicity when pre-treated with MSC cm. Global gene expression changes induced in neurons before and after treatment with MSC cm and/or NMDA were investigated using a cDNA spotted macroarray filter. Four samples were analysed in duplicate: neurons alone (untreated), neurons+MSC cm, neurons+NMDA, neurons+MSC cm+NMDA.
2011-05-01 | E-GEOD-26279 | biostudies-arrayexpress
Project description:This experiment comprises RNA-seq data used to study evolutionary differences between humans and mice in neuronal activity-dependent transcriptional responses. Activity-dependent transcriptional responses in developing human stem cell-derived cortical neurons were compared with those induced in developing primary- or stem cell-derived mouse cortical neurons 4 hours after KCl-induced membrane depolarisation. Activity-dependent transcriptional responses were also measured in aneuploid mouse neurons carrying human chromosome 21, allowing study of the regulation of Hsa21 genes, plus their mouse orthologs, side-by-side in the same cellular environment of a mouse primary neuron.
2017-02-16 | E-MTAB-5489 | biostudies-arrayexpress
Project description:Identification of activity-induced genes in cortical inhibitory neurons (RNA-Seq)
| PRJNA240170 | ENA
Project description:Inhibition of proteasome degradation pathway has been implicated in neuronal cell death leading to neurodegenerative diseases such as ParkinsonM-bM-^@M-^Ys disease and AlzheimerM-bM-^@M-^Ys disease. Pharmacological proteasomal inhibitors such as lactacystin can induce apoptosis in cultured mouse cortical neurons through the activation of caspase-3. Furthermore, proteasomal inhibitors are also reported to mediate deleterious alterations in cell cycle regulation, inflammatory processes and protein aggregation and trigger the cell death pathway. We discovered by microarray analysis that lactacystin treatment modulates the expression of both potentially neuroprotective as well as pro-apoptotic genes in neurons. However, the genes, upon transcriptional modulation, contribute to proteasomal inhibition-induced apoptosis, remains unidentified. By employing microarray analysis to decipher the time-dependent changes in transcription of these genes in cultured cortical neurons, we discovered different groups of genes were transcriptionally regulated at different phases of lactacystin-induced cell death. Microarray analysis was carried out using 10 murine genome U74A and U74Av2 Genechips array (Affymetrix, Santa Clara, CA). The assignment of the arrays (GeneChip) was as follows: Control at 24 h (n=2), 48 h (n=2); exposure to 1 M-NM-<M lactacystin for 24 h (n=3) and 48 h (n=3).
2012-01-03 | E-GEOD-22465 | biostudies-arrayexpress