Gene expression profile at single neuron level of mouse hippocampal neuron, sampled from ex vivo acute brain slice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE262930 | GEO | 2024/04/06
REPOSITORIES: GEO
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Project description:Gene expression profile at single neuron level of mouse hippocampal neuron, sampled from ex vivo acute brain slice
| PRJNA1094930 | ENA
Project description:Dorsal root ganglion neurons are the primary neurons of the sensory afferent pathway and are a heterogeneous population. Dorsal root ganglion neurons exhibit a wide range of terminal morphologies, complex central projection patterns, and different physiological properties, which allow them to adapt to various sensory stimulation modalities and transmit the corresponding sensory information to the central nervous system. Here, we used single-cell sequencing technology to explore the mechanisms behind the differences in axonal lengths in DRG neurons cultured in vitro. The single-cell sequencing data grouped by axon length were compared and analyzed to find core genes that may be closely related to axon length in a list of differentially expressed genes that significantly change with axon length; as well as to explore whether these genes also play an important role in the process of axon regeneration after peripheral nerve injury.
2022-10-01 | GSE205983 | GEO
Project description:Circadian neurons within animal brains orchestrate myriad physiological processes and behaviors, but the contribution of these neurons to the regulation of sleep is not well understood. To address this deficiency, we leveraged single-cell RNA sequencing to generate a new and now comprehensive census of transcriptomic cell types of Drosophila clock neurons. We focused principally on the enigmatic DN3s, which constitute most fly brain clock neurons and were previously almost completely uncharacterized. These DN3s are organized into 12 clusters with unusual gene expression features compared to the more well-studied clock neurons. We further show that previously uncharacterized DN3 subtypes promote sleep through a G protein–coupled receptor, TrissinR. Our findings indicate an intricate regulation of sleep behavior by clock neurons and highlight their remarkable diversity in gene expression and functional properties.
2024-11-20 | GSE276175 | GEO
Project description:This study aimed to characterize the transcriptomes of adult retinal ganglion cells (RGCs). The physiological properties of these cells were characterized first in non-dissociated retinal tissue. With that information recorded, the cells were isolated for transcriptome profiling.
2019-11-01 | GSE115379 | GEO
Project description:To determine the physiological roles of NCOA4 and NCOA4-mediated ferritinophagy in hippocampal neurons, NCOA4 was depleted using siRNA and desferrioxamine (DFO; 100 µM, 24 h) was added to restrict iron availability. Cells were treated for NCOA4 depletion, iron restriction, or both, and then the transcriptome profiles acquired from RNA-seq were compared with those of control (scramble siRNA-treated) cells.
2022-12-30 | GSE211931 | GEO
Project description:Gene expression changes induced by alpha-secretase cleaved amyloid precursor protein (sAPPalpha) in organotypic hippocampal slice cultures of male, postnatal day 15 mice (C57B6/SJL). Hippocampal slice cultures were treated with phosphate buffered saline (GSM26700, GSM26701, GSM26702) or 1 nM sAPPalpha (GSM26703, GSM26704, GSM26705) for 24 h. Each sample consists of total RNA isolated from 8-12 slices from 4 mice. Data were analyzed with MAS 5.0 and scaled to 2500. sAPPalpha induces the amyloid sequestration protein transthyretin, insulin-like growth factor 2, insulin-like growth factor binding protein 2, and other genes involved in protective pathways such as apoptosis inhibition, detoxification, and retinol transport. See Stein, TD, Anders, NJ, DeCarli, C, Chan, SL, Mattson, MP, and Johnson JA. Neutralization of transthyretin reverses the neuroprotective effects of secreted APP in APPSw mice resulting in tau phosphorylation and loss of hippocampal neurons: support for the amyloid hypothesis. J Neurosci. in press.
2007-10-10 | E-GEOD-1555 | biostudies-arrayexpress
Project description:Neocortical hyperexcitability is a prominent feature of inherited and sporadic amyotrophic lateral sclerosis (ALS) and is inversely correlated with patient survival. Cell-type specific changes in neuronal function have been proposed to underlie these functional abnormalities and contribute to the selective degeneration of corticospinal and spinal motor neurons. We analyzed the physiological properties of distinct classes of neurons in the motor cortex of hSOD1G93A mice and found that they exhibit robust physiological changes that depend on disease stage. Targeted recordings and in vivo calcium imaging revealed that neurons adapt their properties to normalize cortical excitability as disease progresses. Although different neuron classes exhibited similar functional changes, transcriptional profiling and pharmacological manipulations indicate that the molecular mechanisms underlying these changes are cell-type specific. These widespread, stage-dependent alterations in neuronal function in ALS mice highlight the dynamic changes cortical circuits experience during neurodegeneration and expand potential therapeutic strategies for normalizing circuit function.
2017-09-30 | GSE101391 | GEO
Project description:Gene expression changes induced by alpha-secretase cleaved amyloid precursor protein (sAPPalpha) in organotypic hippocampal slice cultures of male, postnatal day 15 mice (C57B6/SJL). Hippocampal slice cultures were treated with phosphate buffered saline (GSM26700, GSM26701, GSM26702) or 1 nM sAPPalpha (GSM26703, GSM26704, GSM26705) for 24 h. Each sample consists of total RNA isolated from 8-12 slices from 4 mice. Data were analyzed with MAS 5.0 and scaled to 2500. sAPPalpha induces the amyloid sequestration protein transthyretin, insulin-like growth factor 2, insulin-like growth factor binding protein 2, and other genes involved in protective pathways such as apoptosis inhibition, detoxification, and retinol transport. Keywords = Alzheimer's disease Keywords = neuroprotection Keywords = sAPPalpha
2004-07-30 | GSE1555 | GEO
Project description:Newborn neurons enter an extended maturation stage, during which they acquire excitability characteristics crucial for development of presynaptic and postsynaptic connectivity. In contrast to earlier specification programs, little is known aboutthe regulatory mechanisms that control neuronal maturation. The Pet-1 ETS (E26 transformation-specific) factor is continuously expressed in serotonin (5-HT) neurons and initially acts in postmitotic precursors to control acquisition of 5-HT transmitter identity. Using a combination of RNA sequencing, electrophysiology, and conditional targeting approaches, we determined gene expression patterns in maturing flow-sorted 5-HT neurons and the temporal requirements for Pet-1 in shaping these patterns for functional maturation of mouse 5-HT neurons. We report a profound disruption of postmitotic expression trajectories in Pet-1 / neurons, which prevented postnatal maturation of 5-HT neuron passive and active intrinsic membrane properties, G-protein signaling, and synaptic responses to glutamatergic, lysophosphatidic, and adrenergic agonists. Unexpectedly, conditional targeting revealed a postnatal stage-specific switch in Pet-1 targets from 5-HT synthesis genes to transmitter receptor genes required for afferent modulation of 5-HT neuron excitability. 5-HT1a autoreceptor expression depended transiently on Pet-1, thus revealing an early postnatal sensitive period for control of 5-HT excitability genes. Chromatin immunoprecipitation followed by sequencing revealed that Pet-1 regulates 5-HT neuron maturation through direct gene activation and repression. Moreover, Pet-1 directly regulates the 5-HT neuron maturation factor Engrailed 1, which suggests Pet-1 orchestrates maturationthrough secondary postmitotic regulatoryfactors. The early postnatal switch in Pet-1targets uncovers a distinct neonatal stage-specific function for Pet-1, during which it promotes maturation of 5-HT neuron excitability. 5-HT neuron mRNA profiles of E11.5, E15.5, and postnatal (P1-P3) wild type (WT) and Pet-1-/- mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500. Myc-tagged Pet-1 ChIP-seq was performed on E12.5 to E14.5 hindbrains and sequencing using NextSeq 500.
2016-01-08 | E-GEOD-74315 | biostudies-arrayexpress
Project description:BackgroundThiamine (vitamin B1) is a cofactor for enzymes of central energy metabolism and its deficiency (TD) impairs oxidative phosphorylation, increases oxidative stress, and activates inflammatory processes that can lead to neurodegeneration. Wernicke-Korsakoff syndrome (WKS) is a consequence of chronic TD, which leads to extensive neuronal death, and is associated with neuropathological disorders, including cognitive deficits and amnesia. The hippocampus is one of the brain areas most affected by WKS. B1 replacement may not be enough to prevent the irreversible cognitive deficit associated with WKS.Materials and methodsAn organotypic hippocampal slice culture (OHC) model was developed to investigate, using immunofluorescence and confocal microscopy and transcriptome analysis, the molecular mechanisms underlying the neurodegeneration associated with TD. The effect of anti-inflammatory pharmacological intervention with resveratrol (RSV) was also assessed in B1-deprived OHCs.ResultsIn OHCs cultured without B1, neuronal density decayed after 5 days and, on the 7th day, the epigenetic markings H3K4me3 and H3K9me3 were altered in mature neurons likely favoring gene transcription. Between the 7th and the 14th day, a pulse of neurogenesis was observed followed by a further massive neuron loss. Transcriptome analysis at day nine disclosed 89 differentially expressed genes in response to B1 deprivation. Genes involved in tryptophan metabolism and lysine degradation KEGG pathways, and those with Gene Ontology (GO) annotations related to the organization of the extracellular matrix, cell adhesion, and positive regulation of synaptic transmission were upregulated. Several genes of the TNF and FoxO signaling pathways and with GO terms related to inflammation were inhibited in response to B1 deprivation. Nsd1, whose product methylates histone H3 lysine 36, was upregulated and the epigenetic marking H3K36me3, associated with negative regulation of neurogenesis, was increased in neurons. Treating B1-deprived OHCs with RSV promoted an earlier neurogenesis pulse.ConclusionNeuroregeneration occurs in B1-deficient hippocampal tissue during a time window. This phenomenon depends on reducing neuroinflammation and, likely, on metabolic changes, allowing acetyl-CoA synthesis from amino acids to ensure energy supply via oxidative phosphorylation. Thus, neuroinflammation is implicated as a major regulator of hippocampal neurogenesis in TD opening a new search space for treating WKS.
| S-EPMC9664832 | biostudies-literature