Transcription profiling of mouse hippocampal slices after NMDA or forskolin-rolipram-0 Mg2+ or bicuculline treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Luis Valor
PROVIDER: E-MEXP-1184 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Kinase networks integrate profiles of N-methyl-D-aspartate receptor-mediated gene expression in hippocampus.
Coba Marcelo P MP Valor Luis M LM Kopanitsa Maksym V MV Afinowi Nurudeen O NO Grant Seth G N SG
The Journal of biological chemistry 20080923 49
The postsynaptic N-methyl-d-aspartate (NMDA) receptor activates multiple kinases and changes the phosphorylation of many postsynaptic proteins organized in signaling networks. Because the NMDA receptor is known to regulate gene expression, it is important to examine whether networks of kinases control signaling to gene expression. We examined the requirement of multiple kinases and NMDA receptor-interacting proteins for gene expression in mouse hippocampal slices. Protocols that induce long-term ...[more]
Similar Datasets
Project description:Advancing the quest for new drug targets demands the development of innovative plasma membrane proteome research strategies applicable to small, functionally defined tissue samples. Biotinylation of acute tissue slices and streptavidin pull-down followed by shotgun proteomics allowed the selective extraction and identification of ? 1600 proteins of which > 60% are known to be associated to the plasma membrane according to GO annotations, including (G-protein coupled) receptors, ion channels and transporters, and this from mm3-scale tissue.
2022-02-22 | PXD002227 | Pride
Project description:With improved whole-cell isolation protocols, we performed single-cell RNA sequencing (scRNA-seq) and profiled the transcriptomes from adult non-human primate brain. We identified discriminative cell populations with canonical and novel markers. Cross-species projection demonstrated the evolutionary conservation among mouse, monkey, and human. This dataset serves as a detailed transcriptomic atlas for understanding the adult primate central nervous system.
2022-05-07 | E-MTAB-10225 | biostudies-arrayexpress
Project description:Previous work demonstrated that the developmental pruning of dendritic spines requires autophagy. This developmental process is facilitated by long-term depression (LTD)-like mechanisms, inviting the speculation that LTD, a fundamental form of plasticity, itself requires autophagy. Here, we show that LTD-inducing activation of NMDA receptors or metabotropic glutamate receptors triggers the rapid initiation of autophagy in postsynaptic dendrites. Dendritic autophagic vesicles (AVs) act in parallel with the endocytic machinery to remove AMPAR subunits from the surface and rapidly degrade them and their scaffold PSD95. Moreover, during NMDAR-LTD, key postsynaptic proteins are sequestered for autophagic degradation, as revealed by quantitative proteomic profiling of purified AVs. In turn, pharmacological inhibition of AV biogenesis, or conditional ablation of atg5 in pyramidal neurons abolishes LTD and instead triggers sustained potentiation in the hippocampus. These deficits in synaptic plasticity are recapitulated by knockdown of atg5 specifically in postsynaptic pyramidal neurons in the CA1 area. Conducive to the role of synaptic plasticity in behavioral flexibility, mice with autophagy deficiency in excitatory neurons exhibit altered response in reversal learning. Therefore, local assembly of the autophagic machinery in dendrites ensures the degradation of postsynaptic components and facilitates LTD expression.
2022-01-10 | PXD030079 | Pride
Project description:To isolation of high-yield and viable brain cells including neurons and neural progenitors from adult primate brains, we have developed a reproducible whole-cell dissociation procedure for isolation of primary brain cells from adult and aged primates, with high-yield progenitor, immature and mature neural cells. We verified the viability of isolated cells and identified the main cell type with canonical markers. Furthermore, isolated primate neural progenitors by this our protocol is viable enough for culturing in vitro. This dataset is a detailed single cell RNA-sequencing results for two primate brain regions: primary visual cortex and prefrontal cortex.
2023-06-08 | E-MTAB-12399 | biostudies-arrayexpress
Project description:To increase our understanding of psoriasis, we utilized RNA-seq to assay the transcriptomes of lesional psoriatic and normal skin. We sequenced polyadenylated RNA-derived cDNAs from 92 psoriatic and 82 normal punch biopsies, generating an average of ~38 million single-end 80-bp reads per sample. Comparison of 42 samples* examined by both RNA-seq and microarray [GSE13355] revealed marked differences in sensitivity, with transcripts identified only by RNA-seq having much lower expression than those also identified by microarray. RNA-seq identified many more differentially expressed transcripts enriched in immune system processes. Weighted gene co-expression network analysis (WGCNA) revealed multiple modules of coordinately expressed epidermal differentiation genes, overlapping significantly with genes regulated by the long non-coding RNA TINCR, its target gene, staufen-1 (STAU1), the p63 target gene ZNF750, and its target KLF4. Other coordinately expressed modules were enriched for lymphoid and/or myeloid signature transcripts and genes induced by IL-17 in keratinocytes. Dermally-expressed genes were significantly down-regulated in psoriatic biopsies, most likely due to expansion of the epidermal compartment. These results demonstrate the power of WGCNA to elucidate gene regulatory circuits in psoriasis, and emphasize the influence of tissue architecture in both differential expression and co-expression analysis. *The list of 42 samples examined by both RNA-seq and microarray is provided in the 'MAoverlappedsamples.txt'. 92 psoriatic and 82 normal skin samples
2014-01-29 | E-GEOD-54456 | biostudies-arrayexpress
Project description:Borna Disease Virus (BDV) is a neurotropic virus that persistently infects neurons in the central nervous system of various hosts, including rats. Although BDV is known to be an IFN sensitive virus, determination of the cellular mRNA transcript levels revealed the induction of IFN-stimulated genes in organotypic rat hippocampus slice cultures, raising the question how BDV evades this innate immune response. Using rat Mx protein as a specific marker for IFN-induced gene products, we could show that neurons lack detectable levels of Mx in these BDV infected cultures, whereas astrocytes and microglial cells were Mx positive. Neurons remained Mx negative after treatment of uninfected hippocampus cultures as well as primary dissociated neuronal cultures with high concentrations of IFN-M-NM-1. This non-responsiveness correlated with a lack of a detectable nuclear translocation of pSTAT1 in rat neurons. Consistently, IFN treatment of BDV-infected rat neurons did not prevent the establishment of a viral persistence in the neuronal tissue. However, IFN treatment efficiently prevented vesicular stomatitis virus (VSV) replication, indicating that these cells can mount a weak innate immune response. In contrast, IFN treatment of mouse neurons resulted in the upregulation of Mx1 proteins and inhibition of BDV replication, indicating species-specific differences in the IFN response in neurons between mice and rats. Rat neurons may therefore represent the ideal cell type for BDV to evade the innate immune in the central nervous system. To determine the mRNA levels in the hippocampal slice cultures after BDV infection in Sprague Dawley and Lewis rats Hippocampal slice cultures were prepared from newborn Lewis and SD rats (P0-P2). Half of the samples remained uninfected, whereas the other half was infected with 1000 focus forming units (FFU) of BDV strain He/80. Total RNA from a pool of 12 slice cultures was prepared
2013-06-26 | E-GEOD-41540 | biostudies-arrayexpress
Project description:In this study we sought to determine the effect of overexpressing the SUMOylation E2 conjugase Ubc9 on the response of murine Neural Stem Cells (NSCs) to oxygen-glucose-deprivation and restoration of oxygen/glucose (OGD/ROG). We established stably-expandable lines of NSCs from the subventricular zones (SVZ) of adult wild-type mice (WT NSCs) and Ubc9-overexpressing mice (Ubc9 NSCs) and profiled their transcriptional changes in response to OGD/ROG as well as in response to differentiation.
2019-04-11 | E-MTAB-7428 | biostudies-arrayexpress
Project description:Insults to the cerebral cortex, such as trauma, ischemia or infections, may result in the development of epilepsy, one of the most common neurological disorders. Previous studies have suggested that perturbations in neurovascular integrity and breakdown of the blood-brain barrier (BBB) lead to neuronal hypersynchronization and epileptiform activity, but the underlying mechanisms are unknown. As with BBB opening, treatment with albumin or with TGF-?1 results in the development of hypersynchronized epileptiform activity. Given the latent period before the appearance of epileptiform activity, we hypothesized the underlying mechanism is a transcriptional response which would be similar for BBB breakdown and exposure to albumin or TGF-?1. In search of a common pathway and transcriptional activation pattern we performed a genome wide analysis. Genomic expression analyses demonstrated similar expression patterns for BBB opening, albumin and TGF-?1 exposure. Most importantly, TGF-? pathway blockers suppressed most albumin-induced transcriptional changes. RNA was extracted from cortical regions of rats treated with sodium deoxycholate (DOC, to induce BBB opening), albumin or TGF-?1 for various durations (7/8, 24, 48hr). Control RNA was extracted from a sham-operated animal and one array was run for each treatment and time point A second set of animals (labeled as Set 2) was treated with either albumin (n=3) or albumin in the presence of TGF-? receptor blockers (n=4; TGF-?R1 kinase activity inhibitor SB431542 and TGF-?R2 antibody) and sacrificed 24 hr following treatment. Sham-operated animals served as controls (n=2).
2009-07-15 | E-GEOD-12304 | biostudies-arrayexpress
Project description:Fast-spiking (FS) interneurons are important elements of neocortical circuitry that constitute the primary source of synaptic inhibition in adult cortex and impart temporal organization on ongoing cortical activity. The highly specialized intrinsic membrane and firing properties that allow cortical FS interneurons to perform these functions are attributable to equally specialized gene expression, which is ultimately coordinated by cell-type-specific transcriptional regulation. Although embryonic transcriptional events govern the initial steps of cell-type specification in most cortical interneurons, including FS cells, the electrophysiological properties that distinguish adult cortical cell types emerge relatively late in postnatal development, and the transcriptional events that drive this maturational process are not known. To address this, we used mouse whole-genome microarrays and whole-cell patch clamp to characterize the transcriptional and electrophysiological maturation of cortical FS interneurons between postnatal day 7 (P7) and P40. We found that the intrinsic and synaptic physiology of FS cells undergoes profound regulation over the first 4 postnatal weeks and that these changes are correlated with primarily monotonic but bidirectional transcriptional regulation of thousands of genes belonging to multiple functional classes. Using our microarray screen as a guide, we discovered that upregulation of two-pore K leak channels between P10 and P25 contributes to one of the major differences between the intrinsic membrane properties of immature and adult FS cells and found a number of other candidate genes that likely confer cell-type specificity on mature FS cells. Experiment Overall Design: We characterized the transcriptional maturation of genetically labeled FS interneurons in mouse S1 cortex using whole-genome microarrays.mRNA was harvested from manually sorted GFPexpressing neurons dissociated from acutely prepared brain slices at a range of developmental time points (P7, P10, P15, P25, and P40) and subsequently reverse transcribed, amplified, labeled, and hybridized to Affymetrix 430 2.0 whole-genome microarrays (three microarrays from three different animals per condition). We used the G42 transgenic mice described by Chattopadhyaya et al. (2004) for all experiments.
2009-09-17 | E-GEOD-17806 | biostudies-arrayexpress
Project description:We carried out time-course RNA-Seq in control and prion-exposed BL6 organotypic cerebellar slices treated with or without FabPOM2.
2022-04-20 | E-MTAB-11635 | biostudies-arrayexpress