Mus musculus
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ABSTRACT:
PROVIDER: PRJNA106639 | ENA |
REPOSITORIES: ENA
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Project description:XBP1 is a transcription factor that is induced by unconventional splicing associated with endoplasmic reticulum stress and plays a role in development of liver and plasma cells. We previously reported that brain derived neurotrophic factor (BDNF) leads to splicing of XBP1 mRNA in neurites, and that XBP1 is required for BDNF-induced neurite extension and branching. To search for the molecular mechanisms of how XBP1 plays a role in neural development, comprehensive gene expression analysis was performed in primary telencephalic neurons obtained from Xbp1 knockout mice at embryonic day 12.5. By searching for the genes induced by BDNF in wild type neurons but this induction was reduced in Xbp1 knockout mice, we found that upregulation of three GABAergic markers, somatostatin (Sst), neuropeptide Y (Npy), and calbindin (Calb1), were compromised in Xbp1 knockout neurons. Attenuated induction of Npy and Calb1 was confirmed by quantitative RT-PCR. In neurons lacking in Xbp1, upregulation of GABAergic markers was attenuated. Impaired BDNF-induced neurite extension in Xbp1 knockout neurons might be mediated by disturbed BDNF-induced differentiation of GABAergic interneurons. Keywords: time-cource, genetic modification
2008-09-25 | GSE11322 | GEO
Project description:XBP1 is a transcription factor that is induced by unconventional splicing associated with endoplasmic reticulum stress and plays a role in development of liver and plasma cells. We previously reported that brain derived neurotrophic factor (BDNF) leads to splicing of XBP1 mRNA in neurites, and that XBP1 is required for BDNF-induced neurite extension and branching. To search for the molecular mechanisms of how XBP1 plays a role in neural development, comprehensive gene expression analysis was performed in primary telencephalic neurons obtained from Xbp1 knockout mice at embryonic day 12.5. By searching for the genes induced by BDNF in wild type neurons but this induction was reduced in Xbp1 knockout mice, we found that upregulation of three GABAergic markers, somatostatin (Sst), neuropeptide Y (Npy), and calbindin (Calb1), were compromised in Xbp1 knockout neurons. Attenuated induction of Npy and Calb1 was confirmed by quantitative RT-PCR. In neurons lacking in Xbp1, upregulation of GABAergic markers was attenuated. Impaired BDNF-induced neurite extension in Xbp1 knockout neurons might be mediated by disturbed BDNF-induced differentiation of GABAergic interneurons. Experiment Overall Design: Brain derived neurotrophic factor (BDNF) effect examined in telencephalon primary cultures from Xbp1 knockouts and wild-type controls. Experiment Overall Design: Two female Xbp1 +/- mice were mated with male Xbp1 +/- mice, and at embryonic day 12.5 (E12.5) the embryos were dissected. Among the 25 embryos obtained from the 2 pregnant female mice, 6 were genotyped as Xbp1 -/- and 4 were Xbp1 +/+ by a rapid PCR assay using Z-Taq. Telencephalon was dissected from each embryo, and treated with collagenase and trypsin. Six Xbp1 -/- telencephalon samples and 4 Xbp1 +/+ samples were collected together, respectively. Each sample was divided into 15 aliquots, and the cells were subject to low density culture on plastic culture dishes. The neurons were maintained in a serum-free medium (Neurobasal medium supplemented with 0.5 mM glutamine and B27 supplement [Invitrogen]). On the third day in vitro (3 DIV) , neurons in 10 of 15 dishes in each group were stimulated with BDNF (100 ng/ml). On 4 DIV, neurons in 5 dishes stimulated with BDNF (24 hours BDNF treatment) and 5 dishes with no stimulation (0 hour) were lysed to extract total RNA. On 5 DIV, neurons in 5 dishes stimulated with BDNF (48 hours BDNF treatment) were lysed. Experiment Overall Design: Total RNA was extracted using RNAeasy Micro Kit (Qiagen, Hilden, Germany) according to the protocol provided by the manufacturer. The quantity and quality of RNA were measured using NanoDrop ND-1000. Biotin-labeled cRNA for DNA microarray analysis was synthesized using Two Cycle cDNA Synthesis and IVT labeling Kit. The integrity of the cRNA samples was verified using Test3 Array. Each biotin-labeled cRNA sample from one dish was hybridized to a single Affymetrix GeneChip Mouse Genome 430A 2.0 Array, and totally 30 arrays were used. The hybridization signal on the chip was scanned using an HP GeneArray scanner and processed by MAS5. After imported into GeneSpring software, data normalization was performed by dividing each microarray data set by its median value. Probes called as present in at least half of the 30 samples were selected.
2008-10-26 | E-GEOD-11322 | biostudies-arrayexpress
Project description:Induction of cells expressing markers of GABAergic neurons by transcription factors (mRNA)
| PRJNA314496 | ENA
Project description:Induction of cells expressing markers of GABAergic neurons by transcription factors (miRNA)
| PRJNA314495 | ENA
Project description:RNAseq data indicate that in the human brain, most neurons co-express the brain-derived neurotrophic factor (BDNF) receptor TrkB and the Neurotrophin-3 (NT3) receptor TrkC. Because NT3 can also activate TrkB and TrkB is expressed at higher levels compared with TrkC, it has been difficult thus far to explore TrkC-mediated signaling. To this end, neurons were generated from human embryonic stem cells lacking the BDNF receptor TrkB using CRISPR/Cas9. These neurons were found to respond to very low concentrations of NT3, lower than the concentrations of BDNF needed to activate TrkB. In order to compare the transcriptional changes following treatment with NT3 RNA-seq analysis was performed and the results compared with those previously obtained following treatment of wild-type neurons with BDNF Merkouris et al. PMID: 29987039. The results indicate that downstream of TrkC activation, most of the changes in gene expression are similar to those seen after TrkB activation. The results also show that exposure to sub-saturating concentrations of either BDNF or NT3 does not cause receptor downregulation as seen with saturating ligand concentrations and that the receptors can be re-activated.
2022-03-22 | E-MTAB-11566 | biostudies-arrayexpress
Project description:A crucial step in understanding the sleep-control mechanism is to identify sleep neurons. In principle, a neuron could promote sleep by inhibiting wake-promoting neurons. Using rabies virus (RV)-mediated transsynaptic tracing, we identified several brain regions with GABAergic neurons that broadly inhibit multiple wake-promoting neuronal populations, and the most prominent source of GABAergic inputs was found in a posterior part of the CeA. The CeA is known to contain multiple subtypes of GABAergic neurons with distinct molecular markers, projection targets, and functional properties. Using translating ribosome affinity purification (TRAP) RNA-Seq, we identified molecular markers for the canditate sleep-promoting neurons in CeA.
2020-04-06 | GSE121888 | GEO
Project description:Rationale: A previous transcriptome meta-analysis revealed significantly lower levels of corticotropin-releasing hormone (CRH) mRNA in corticolimbic brain regions in major depressive disorder (MDD) subjects. Rodent studies show that cortical CRH is mostly expressed in GABAergic neurons; however, the characteristic features of CRH+ cells in human brain cortex and their association with MDD are largely unknown. Methods: Subgenual anterior cingulate cortex (sgACC) of human subjects without brain disorders were labeled using fluorescent in situ hybridization (FISH) for CRH and markers of excitatory (SLC17A7), inhibitory (GAD1) neurons, as well as markers of other interneuron subpopulations (PVALB, SST, VIP). MDD-associated changes in CRH+ cell density and cellular CRH expression (n=6/group) were analyzed. RNA-sequencing was performed on sgACC CRH+ neurons from comparison and MDD subjects (n=6/group), and analyzed for group differences. Results: About 80% of CRH+ cells were GABAergic and 17.5% were glutamatergic. CRH+ GABAergic neurons co-expressed VIP (52%), SST (7%), or PVALB (7%). MDD subjects displayed lower CRH mRNA levels in GABAergic neurons relative to comparison subjects without changes in cell density. CRH+ neurons show transcriptomic profile suggesting lower excitability and less GABA release and reuptake. Further analyses suggested that these molecular changes are not mediated by altered glucocorticoid feedback and potentially occur downstream for a common modulator of neurotrophic function. Summary: CRH+ cells in human sgACC are a heterogeneous population of GABAergic neurons, although largely co-expressing VIP. MDD is associated with reduced markers of inhibitory function of CRH+ neurons.
2022-02-22 | GSE193417 | GEO
Project description:Certain neuron types fire spontaneously at high rates, an ability that is crucial for their function in brain circuits. The spontaneously active GABAergic neurons of the substantia nigra pars reticulata (SNr), a major output of the basal ganglia, provide tonic inhibition of downstream brain areas. A depolarizing "leak" current supports this firing pattern, but its molecular basis remains poorly understood. To understand how SNr neurons maintain tonic activity, we used single-cell RNA sequencing to determine the transcriptome of individual SNr neurons. We discovered that SNr neurons express the sodium leak current, NaLCN and that SNr neurons lacking NaLCN have impaired spontaneous firing. RNA sequencing profiles from 87 GFP-positive GABAergic SNr neurons and 9 GFP-negative SNr cells were carried out. However only 80 samples that passed initial quality control and that were included in the data processing are represented in this record.
2016-05-13 | E-GEOD-78521 | biostudies-arrayexpress
Project description:Induction of cells expressing markers of GABAergic neurons by transcription factors
| PRJNA314491 | ENA
Project description:Expression profiling in cortical GABAergic neurons at neonate
| PRJNA360536 | ENA