Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112691 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mice lacking the growth associated protein, GAP-43, (KO) show multiple deficits in forebrain axon guidance and cortical cell differentiation (Donovan and McCasland, 2005). As a result, GAP-43 KO mice fail to form barrels in mouse somatosensory cortex (S1) (Maier et al., 1999). GAP-43 heterozygous (HZ) mice show abnormalities in axonal pathfinding and show larger than normal barrels in layer IV S1 due to widely branched thalamocortical afferents (TCAs). Regardless of abnormalities during early development, HZ barrels become indistinguishable from WT by postnatal day 26. One explanation for these findings is that compensatory mechanisms may be activated in GAP-43 HZ cortex. We have used mRNA microarray expression analysis to gain a more comprehensive view of genes involved in GAP-43 signaling during barrel map formation. Using laser microdissection , cortical cells of the barrel cortex were excised, RNA extracted and used in GeneChip analysis. Expression profiling and functional gene group analysis of RNA from WT, HZ, and KO cortex at postnatal day 5 was performed. We identified thousands of transcripts differentially expressed across the genotypes. Verification of selected changes in gene expression was accomplished using in situ hybridization. Our results suggest an adaptive modification in transcript expression of genes involved in cell-cell communication and synaptogenesis. These modifications appear important in forward and reverse signaling as well as maintaining synchrony between the cells. Compensatory up- and down regulation of synapse-associated genes may explain the reverse in HZ phenotype from P7 to P26. Moreover, these findings provide new insight into the role GAP-43 plays in several pathways associated with synaptogenesis and trans-synaptic signaling. Experiment Overall Design: 3 replicate RNA samples were prepared from laser microdissected barrel cortex samples of WT, HZ and KO mice at a single timepoint (postnatal day 5)
2009-06-08 | E-GEOD-12687 | biostudies-arrayexpress
Project description:Mice lacking the growth associated protein, GAP-43, (KO) show multiple deficits in forebrain axon guidance and cortical cell differentiation (Donovan and McCasland, 2005). As a result, GAP-43 KO mice fail to form barrels in mouse somatosensory cortex (S1) (Maier et al., 1999). GAP-43 heterozygous (HZ) mice show abnormalities in axonal pathfinding and show larger than normal barrels in layer IV S1 due to widely branched thalamocortical afferents (TCAs). Regardless of abnormalities during early development, HZ barrels become indistinguishable from WT by postnatal day 26. One explanation for these findings is that compensatory mechanisms may be activated in GAP-43 HZ cortex. We have used mRNA microarray expression analysis to gain a more comprehensive view of genes involved in GAP-43 signaling during barrel map formation. Using laser microdissection , cortical cells of the barrel cortex were excised, RNA extracted and used in GeneChip analysis. Expression profiling and functional gene group analysis of RNA from WT, HZ, and KO cortex at postnatal day 5 was performed. We identified thousands of transcripts differentially expressed across the genotypes. Verification of selected changes in gene expression was accomplished using in situ hybridization. Our results suggest an adaptive modification in transcript expression of genes involved in cell-cell communication and synaptogenesis. These modifications appear important in forward and reverse signaling as well as maintaining synchrony between the cells. Compensatory up- and down regulation of synapse-associated genes may explain the reverse in HZ phenotype from P7 to P26. Moreover, these findings provide new insight into the role GAP-43 plays in several pathways associated with synaptogenesis and trans-synaptic signaling.
2009-06-01 | GSE12687 | GEO
Project description:Understanding the mechanisms that drive TDP-43 pathology is integral to combating amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Here we generated a longitudinal quantitative proteomic map of the cortex from the cytoplasmic TDP-43 rNLS8 mouse model of ALS and FTLD and developed a complementary open-access webtool, TDP-map (https://shiny.rcc.uq.edu.au/TDP-map/). We identified distinct protein subsets enriched for diverse biological pathways with temporal alterations in protein abundance, including increases in protein folding factors prior to disease onset. This included increased levels of DnaJ homolog subfamily B member 5, DNAJB5, which also co-localized with TDP-43 pathology in diseased human motor cortex. DNAJB5 over-expression decreased TDP-43 aggregation in cell and cortical neuron cultures, and knockout of Dnajb5 exacerbated motor impairments caused by AAV-mediated cytoplasmic TDP-43 expression in mice. Together, these findings reveal molecular mechanisms at distinct stages of ALS and FTLD progression and suggest that protein folding factors could be protective in disease.
2024-01-31 | PXD042382 | Pride
Project description:The retinoic acid orphan receptor alpha (RORα) is well known for its role in cerebellar development and maturation as revealed in the stagerrer (Stg) mutant mouse line. However it’s potential involvement for the development of other brain regions has not been assessed. Here we describe a new role of RORα in the development of the thalamic and cortical circuits that leads to the assembly of columnar barrel structures in the primary somatosensory cortex. Microarray analyses comparing gene expression in the thalamus and cortex of the Stg, showed a down-regulation of genes that have been involved in the control of TCA or cellular maturation of layer IV neurons. Overall, our study outlines a new role of RORα for the coordinated maturation of the thalamus and cortex during early postnatal life, and shows that it is required to initiate the transcription of genes involved in barrel formation.
2017-09-30 | GSE80317 | GEO
Project description:Microglia tightly interact with brain capillaries and regulate blood brain barrel permeability in pathological conditions. However, it is still unknown whether and how microglia regulate CBF in homeostatic condition. Here we show microglia directly regulate cerebral blood flow (CBF) and neurovascular coupling. Conditional knockout of microglial CD39 resulted in CBF hyper perfusion, reduced ATP induced CBF increase, impaired neurovascular coupling by whisker stimulation and reduced whisker stimulation induced adenosine increase in barrel cortex. Out data suggest that microglia is an important player for CBF regulation.
2023-07-01 | GSE223314 | GEO
Project description:Bulk RNA sequencing of Brain Endothelial Cells from brain regions that underwent 3 hours of DREADDs-mediated glutamatergic activation or silencing compared to respective littermate controls or volitional whisker-mediated barrel cortex activation compared to no whisker controls.
2020-08-24 | GSE156689 | GEO
Project description:Experience-dependent plasticity (EDP) is essential for anatomical and functional maturation of sensory circuits during development and can be readily studied is the rodent barrel cortex. Using this model we aimed to uncover changes on the transcriptome level and applied RNA sequencing upon altered sensory experience in juvenile mice in a cortical column and layer specific manner. From column- and layer-specific barrel cortical tissue, high quality RNA was purified and sequenced. The current dataset entails an average of 50 million paired-end reads per sample, 75 base pairs in length.
2017-08-17 | GSE90929 | GEO
Project description:Analysis of astrocyte gene expression across postnatal development in the mouse visual cortex, spanning the time of synaptogenesis and synapse maturation.
2021-10-08 | GSE161398 | GEO
Project description:Mus musculus strain:C57 | isolate:barrel cortex Raw sequence reads
| PRJNA375131 | ENA
Project description:To examine the hypothesis that lncRNA expression varies with age, potentially paralleling 25 known developmental trends in synaptogenesis, myelination, and energetics, we quantified levels of nearly 6000 lncRNAs in 36 surgically resected human neocortical samples (primarily derived from temporal cortex) spanning infancy to adulthood. One-color (Alexa 555 green) microarray experiment was performed separately on each of the 36 surgically-resected human neocortical samples (primarily derived from temporal cortex) spanning infancy to adulthood. 8 probes per gene and 5 on-chip replicates for each probe.
2013-01-19 | E-GEOD-43639 | biostudies-arrayexpress