Molecular states underlying neuronal cell type development and plasticity in the whisker cortex
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PROVIDER: PRJNA1157766 | ENA |
REPOSITORIES: ENA
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Project description:Mouse whisker somatosensory cortex (wS1) is a major model system to study the experience-dependent plasticity of cortical neuron physiology, morphology, and sensory coding. However, the role of sensory experience in regulating neuronal cell type development and gene expression in wS1 remains poorly understood. We assembled and annotated a transcriptomic atlas of wS1 during postnatal development comprising 45 molecularly distinct neuronal types that can be grouped into eight subclasses of excitatory neurons and four subclasses of inhibitory neurons. Using this atlas, we examined the influence of whisker experience between postnatal day (P) 12, the onset of active whisking, to P22, on the maturation of molecularly distinct cell types. During this developmental period, when whisker experience was normal, ~250 genes were regulated in a neuronal subclass-specific fashion. At the resolution of neuronal types, we found that only the composition of layer (L) 2/3 glutamatergic neuronal types, but not other neuronal types, changed substantially between P12 and P22. These compositional changes resemble those observed previously in the primary visual cortex (V1), and the temporal gene expression changes were also highly conserved between the two regions. In contrast to V1, however, cell type maturation in wS1 is likely independent of sensory experience, as 10-day full-face whisker deprivation had no influence on the transcriptomic identity and composition of L2/3 neuronal types. A one-day competitive whisker deprivation protocol also did not affect cell type identity but induced moderate changes in plasticity-related gene expression. Thus, developmental maturation of cell types is similar in V1 and wS1, but sensory deprivation has a minimal effect on cell type development in wS1.
2024-11-22 | GSE276528 | GEO
Project description:Thiele2013 - Cerebral cortex neuronal cells
The model of cerebral cortex neuronal cells metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
Recon 2 we predicted changes in metabolite biomarkers for 49 inborn errors of metabolism with 77% accuracy when compared to experimental data. Mapping metabolomic
data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110033
.
To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
2005-01-01 | MODEL1310110033 | BioModels
Project description:Caloric restriction and acute fasting are known to reduce seizures but through unclear mechanisms. In this study, we demonstrate that mTORC1 signaling is reduced after acute fasting of mice. In neurons, mTORC1 is most sensitive to withdrawal of leucine, arginine, and glutamine, which is dependent on DEPDC5. We performed metabolomic analysis of brain cortex from neuronal specific Depdc5 knockout in fed and fasting state. The Depdc5 neuronal specific knockout mice are resistant to sensing significant fluctuations in brain amino acid levels after fasting. These results establish that acute fasting reduces seizure susceptibility in a DEPDC5-dependent manner.
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Project description:Turnover and exchange of nucleosomal histones and their variants, a process long believed to be static in post-replicative cells, remains largely unexplored in brain. Here, we describe a novel mechanistic role for HIRA (histone cell cycle regulator) and proteasomal degradation associated histone dynamics in the regulation of activity-dependent transcription, synaptic connectivity and behavior. We uncover a dramatic developmental profile of nucleosome occupancy across the lifespan of both rodents and humans, with the histone variant H3.3 accumulating to near saturating levels throughout the neuronal genome by mid-adolescence. Despite such accumulation, H3.3 containing nucleosomes remain highly dynamic–in a modification independent manner–to control neuronal- and glial- specific gene expression patterns throughout life. Manipulating H3.3 dynamics in both embryonic and adult neurons confirmed its essential role in neuronal plasticity and cognition. Our findings establish histone turnover as a critical, and previously undocumented, regulator of cell-type specific transcription and plasticity in mammalian brain. All ChIP-seq samples were generated to test the impact of neuronal activity/adult physiological plasticity on histone turnover in the central nervous system. This was tested in cultured neurons and astrocytes, FACS purified neurons or FACS purified Glia.
2015-06-23 | E-GEOD-69806 | biostudies-arrayexpress
Project description:Turnover and exchange of nucleosomal histones and their variants, a process long believed to be static in post-replicative cells, remains largely unexplored in brain. Here, we describe a novel mechanistic role for HIRA (histone cell cycle regulator) and proteasomal degradation associated histone dynamics in the regulation of activity-dependent transcription, synaptic connectivity and behavior. We uncover a dramatic developmental profile of nucleosome occupancy across the lifespan of both rodents and humans, with the histone variant H3.3 accumulating to near saturating levels throughout the neuronal genome by mid-adolescence. Despite such accumulation, H3.3 containing nucleosomes remain highly dynamic–in a modification independent manner–to control neuronal- and glial- specific gene expression patterns throughout life. Manipulating H3.3 dynamics in both embryonic and adult neurons confirmed its essential role in neuronal plasticity and cognition. Our findings establish histone turnover as a critical, and previously undocumented, regulator of cell-type specific transcription and plasticity in mammalian brain. All RNA-seq samples were generated to test the impact of neuronal activity/adult physiological plasticity on histone turnover turnover mediated alterations in mRNA expression in the central nervous system. This was tested in cultured neurons and astrocytes, and embryonic/adult brain tissues
2015-06-23 | E-GEOD-69807 | biostudies-arrayexpress
Project description:Developmental GABA polarity switch and neuronal plasticity in Bioengineered Neuronal Organoids
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Project description:The effect of neuronal activity on blood-brain barrier function and whether it plays a role in plasticity in the healthy brain remains unclear. We show that neuronal activity induces modulation of microvascular permeability in the healthy brain and that it has a role in local network reorganization. Combining simultaneous electrophysiological recording and vascular imaging with transcriptomic analysis in rats, and functional and BBB-mapping MRI in human subjects we show that prolonged stimulation of the limb induces a focal increase in BBB permeability in the corresponding somatosensory cortex that is associated with long-term synaptic plasticity. We further show that the increased microvascular permeability depends on neuronal activity and involves caveolae-mediated transcytosis and transforming growth factor beta signaling. Our results reveal a role of BBB modulation in cortical plasticity in the healthy brain, highlighting the importance of neurovascular interactions for sensory experience and learning.
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Project description:This study provides the first data on gene expression levels in whisker follicles and in the striatum in relation to MA reward and thereby may accelerate the research on the whisker follicle as an alternative source of biomarkers for the diagnosis of MA use disorder.
2021-08-27 | GSE157112 | GEO
Project description:Brain organoids are promising tools for disease modelling and drug development. For proper neuronal network formation excitatory and inhibitory neurons as well as glia need to co-develop. Here we report the directed differentiation and self-organization of induced pluripotent stem cells in a collagen hydrogel towards a highly interconnected neuronal network in a macroscale tissue format. Bioengineered Neuronal Organoids (BENOs) comprise interconnected excitatory and inhibitory neurons as well as supportive astrocytes and oligodendrocytes. Giant depolarizing potential (GDP)-like events observed within 20-40 days of BENO culture mimic early network activity of the fetal brain. The switch from excitatory to inhibitory GABA activity, and reduced GDPs at >40 day BENO cultures indicate progressive neuronal network maturation. BENOs demonstrate expedited complex network burst development after two months of culture and provide the first evidence for long-term potentiation and plasticity in brain organoids. BENOs exhibit structural and functional properties similar to the fetal brain and thus may be explored as a model to study the development of neuronal plasticity.
2020-07-02 | GSE139101 | GEO