RNA-seq of mouse cortical tissue and astrocytes after anesthesia and induction of neuronal activity
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB63078 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11532808.fastq.gz | Fastqsanger.gz | |||
| ERR11532809.fastq.gz | Fastqsanger.gz | |||
| ERR11532810.fastq.gz | Fastqsanger.gz | |||
| ERR11532811.fastq.gz | Fastqsanger.gz | |||
| ERR11532812.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 72 |
Similar Datasets
Project description:General anesthesia is a common clinical procedure yet can result in long term CNS-adverse effects, particularly in the elderly, or dementia patients. Suppression of cortical activity is a key feature of the anesthetic-induced unconscious state, with activity being a well-described regulator of pathways important for brain health. However the extent to which the effects of anesthesia go beyond simple suppression of neuronal activity is incompletely understood, as are its effects on non-neuronal cell types such as astrocytes, which are important integrators of both neuronal activity and inflammatory signalling. In order to address these questions, we performed a combination of RNA-seq and TRAP-seq (Translating Ribosome Affinity Purification, where astrocyte-specific translating mRNAs are sequenced) on mouse cortical tissue and primary cortical neurons.
2023-08-01 | E-MTAB-13054 | biostudies-arrayexpress
Project description:Astrocytes are implicated in neuronal development, particularly excitatory synaptogenesis, but their genome-wide impact is unclear. Using cell-type specific RNA-seq we show that cortical astrocytes induce widespread transcriptomic changes in developing cortical neurons. Rat cortical neurons were maintained in the presence or absence of mouse astrocytes, RNA-seq performed, and mixed-species RNA-seq reads sorted according to species. Cultures were also treated with TTX to abolish neuronal firing activity, to investigate the effects of the presence or absence activity-dependent signalling.
2024-05-14 | E-MTAB-14070 | biostudies-arrayexpress
Project description:Previous studies have proved that astrocytes may be a key neural substrate that regulates wakefulness and consciousness recovery from general anesthesia, while the exact molecular target in astrocytes is still unclear. Using virus injection and in vivo fiber photometry in mice, we found both activating astrocytes and knocking down astrocytic Kir4.1 in paraventricular thalamus (PVT) promotes the consciousness recovery from sevoflurane anesthesia. Single-cell RNA sequencing of PVT reveals two distinct cellular subtypes of glutamatergic neurons: PVTGRM and PVTChAT neurons. Patch-clamp recording results proved that Astrocytic Kir4.1-mediated modulation of sevoflurane on PVT mainly works on PVTChAT neurons. Moreover, we found that PVTChAT neurons project mainly to the mPFC. This specific paraventricular thalamus to prefrontal cortex projection is involved in recovery of consciousness from sevoflurane anesthesia indirectly through modulation of astrocytes. In summary, our findings support the novel conception that the volatile anesthetic sevoflurane can inhibit PVT astrocytic Kir 4.1 to maintain and/or increase neuronal firing of PVTChAT neurons, which mainly projects to mPFC and promotes consciousness recovery from anesthesia.
2024-07-20 | GSE240388 | GEO
Project description:Neuronal morphogenesis relies on intercellular signaling. Astrocytes release metabolites, trophic, and guidance factors to promote neuronal maturation. In contrast, the mechanisms by which astrocytes could limit and stabilize neuronal connectivity remain less explored. Here, we find cortical astrocytes to express and release S100A6, a Ca2+-binding protein (‘calcyclin’). Simultaneously, the majority of cortical neurons expressed calcyclin-binding protein (CaCyBp), a bona fide binding partner for S100A6. In neurons, CaCyBp maintained the unfolded protein response pathway, thereby controlling proteostasis. When released, S100A6 inhibited CaCyBp-mediated signaling, thus slowing protein turnover, and, consequently, neuritogenesis. S100A6-CaCyBp signaling during gestation was sensitive to the mother’s nu tritional status, particularly eicosapentaenoic acid intake. Thus, a member of the S100 protein family acts as an astroglia-derived morphogen, whose action on neurons is modulated by environmental factors.
2025-09-11 | PXD066923 | Pride
Project description:Astrocytes are implicated in neuronal development, particularly excitatory synaptogenesis, but their genome-wide impact is unclear. Using cell-type specific ChIP-seq we show that cortical astrocytes induce widespread changes in developing cortical neurons in histone marks associated with active open chromatin and repressed/condensed chromatin. Rat cortical neurons were maintained in the presence or absence of mouse astrocytes, ChIP-seq performed, and mixed-species ChIP-seq reads sorted according to species.
2024-05-16 | E-MTAB-14081 | biostudies-arrayexpress
Project description:Isolation of glia from Alzheimer's mice reveals inflammation and dysfunction. Reactive astrocytes and microglia are associated with amyloid plaques in Alzheimer's disease (AD). Yet, not much is known about the molecular alterations underlying this reactive phenotype. To get an insight into the molecular changes underlying AD induced astrocyte and microglia reactivity, we performed a transcriptional analysis on acutely isolated astrocytes and microglia from the cortex of aged controls and APPswe/PS1dE9 AD mice. As expected, both cell types acquired a proinflammatory phenotype, which confirms the validity of our approach. Interestingly, we observed that the immune alteration in astrocytes was relatively more pronounced than in microglia. Concurrently, our data reveal that astrocytes display a reduced expression of neuronal support genes and genes involved in neuronal communication. The microglia showed a reduced expression of phagocytosis and/or endocytosis genes. Co-expression analysis of a human AD expression data set and the astrocyte and microglia data sets revealed that the inflammatory changes in astrocytes were remarkably comparable in mouse and human AD, whereas the microglia changes showed less similarity. Based on these findings we argue that chronically proinflammatory astrocyte and microglia phenotypes, showing a reduction of genes involved in neuronal support and neuronal signaling, are likely to contribute to the neuronal dysfunction and cognitive decline in AD. 2 cell types from 2 conditions: cortical microglia and cortical astrocytes from 15-18 month old APPswe/PS1dE9 mice compared to wildtype littermates. Biological replicates: microglia from APPswe/PS1dE9, N=7, microglia from WT, N=7, astrocytes from APPswe/PS1dE9, N=4, microglia from WT, N=4
2015-11-04 | E-GEOD-74615 | biostudies-arrayexpress
Project description:GFAP and vimentin deficiency alters gene expression in astrocytes and microglia in wild-type mice and changes the transcriptional response of reactive glia in mouse model for Alzheimer's disease. Reactive astrocytes with an increased expression of intermediate filament (IF) proteins Glial Fibrillary Acidic Protein (GFAP) and Vimentin (VIM) surround amyloid plaques in Alzheimer's disease (AD). The functional consequences of this upregulation are unclear. To identify molecular pathways coupled to IF regulation in reactive astrocytes, and to study the interaction with microglia, we examined WT and APPswe/PS1dE9 (AD) mice lacking either GFAP, or both VIM and GFAP, and determined the transcriptome of cortical astrocytes and microglia from 15- to 18-month-old mice. Genes involved in lysosomal degradation (including several cathepsins) and in inflammatory response (including Cxcl5, Tlr6, Tnf, Il1b) exhibited a higher AD-induced increase when GFAP, or VIM and GFAP, were absent. The expression of Aqp4 and Gja1 displayed the same pattern. The downregulation of neuronal support genes in astrocytes from AD mice was absent in GFAP/VIM null mice. In contrast, the absence of IFs did not affect the transcriptional alterations induced by AD in microglia, nor was the cortical plaque load altered. Visualizing astrocyte morphology in GFAP-eGFP mice showed no clear structural differences in GFAP/VIM null mice, but did show diminished interaction of astrocyte processes with plaques. Microglial proliferation increased similarly in all AD groups. In conclusion, absence of GFAP, or both GFAP and VIM, alters AD-induced changes in gene expression profile of astrocytes, showing a compensation of the decrease of neuronal support genes and a trend for a slightly higher inflammatory expression profile. However, this has no consequences for the development of plaque load, microglial proliferation, or microglial activation. 2 cell types from 6 conditions: cortical microglia and cortical astrocytes from 15-18 month old APPswe/PS1dE9 mice compared to wildtype littermates. Biological replicates: microglia from APPswe/PS1dE9, N=7, microglia from WT, N=7, astrocytes from APPswe/PS1dE9, N=4, microglia from WT, N=4
2015-11-04 | E-GEOD-74614 | biostudies-arrayexpress
Project description:Astrocytes are glial cells essential for neuronal plasticity. However, the role of astrocytic cAMP signalling in brain activity and function is still missing. We expressed DdPAC, a photoactivated adenylyl cyclase that increases cAMP upon red light, in cortical astrocytes to investigate its effects. We assessed synaptic transmission using multi-electrode arrays, and molecular changes through proteomic, phosphoproteomic, and metabolic analyses. We also measured brain hemodynamics and analysed motor behaviour in wild-type (WT) and R6/1 Huntington's disease (HD) mice. DdPAC stimulation in cortical astrocytes induced long-term synaptic potentiation in WT mice, which was PKA and NMDAR-dependent but Ca2+-independent. It also triggered PKA-signalling pathways and modulated synaptic and morphology-associated proteins. Further, cAMP signalling increased cortical blood flow and improved motor learning in WT mice but show differential responses in HD mice. Our results unravel the impact of cAMP signalling in astrocytes to synaptic to brain function, and highlight its alterations in HD.
2025-09-18 | PXD054635 | Pride
Project description:Astrocytes are glial cells essential for neuronal plasticity. However, the role of astrocytic cAMP signalling in brain activity and function is still missing. We expressed DdPAC, a photoactivated adenylyl cyclase that increases cAMP upon red light, in cortical astrocytes to investigate its effects. We assessed synaptic transmission using multi-electrode arrays, and molecular changes through proteomic, phosphoproteomic, and metabolic analyses. We also measured brain hemodynamics and analysed motor behaviour in wild-type (WT) and R6/1 Huntington's disease (HD) mice. DdPAC stimulation in cortical astrocytes induced long-term synaptic potentiation in WT mice, which was PKA and NMDAR-dependent but Ca2+-independent. It also triggered PKA-signalling pathways and modulated synaptic and morphology-associated proteins. Further, cAMP signalling increased cortical blood flow and improved motor learning in WT mice but show differential responses in HD mice. Our results unravel the impact of cAMP signalling in astrocytes to synaptic to brain function, and highlight its alterations in HD.
2025-09-18 | PXD054633 | Pride
Project description:We report changes in the cortical transcriptome of newborn rat pups after exposure to anesthesia and surgery in the third trimester using unbiased RNA-seq analysis.
2020-11-10 | GSE161122 | GEO