Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior

ABSTRACT: Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior

PROVIDER: PRJNA472565 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7195080_1.fastq.gz	Fastqsanger.gz
	SRR7195080_2.fastq.gz	Fastqsanger.gz
	SRR7195090_1.fastq.gz	Fastqsanger.gz
	SRR7195090_2.fastq.gz	Fastqsanger.gz
	SRR7195100_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 192

Similar Datasets

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior II

Project description:Astrocytes tile the central nervous system, but their functions in neural microcircuits in vivo and their roles in mammalian behavior remain incompletely defined. We used 2-photon laser scanning microscopy (2PLSM), electrophysiology, MINIscopes, RNA-seq and a new genetic approach to characterize the effects of reduced striatal astrocyte Ca2+ signaling in vivo. In wild type mice, reducing striatal astrocyte Ca2+-dependent signaling increased repetitive self-grooming behaviors by altering medium spiny neuron (MSN) activity. The mechanism involved astrocyte-mediated neuromodulation mediated by ambient GABA and was corrected by blocking astrocyte GABA transporter 3 (GAT-3). Furthermore, in a mouse model of Huntington’s disease, dysregulation of GABA and astrocyte Ca2+ signaling accompanied excessive self-grooming, which was relieved by blocking GAT-3. Assessments with RNA-seq revealed astrocyte genes and pathways regulated by Ca2+ signaling in a cell autonomous and non-cell autonomous manner, including Rab11a, a regulator of GAT-3 functional expression. Thus, striatal astrocytes contribute to neuromodulation controlling obsessive-compulsive-like behavior in mice.

2019-05-09 | GSE114756 | GEO

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior I

2019-05-09 | GSE114755 | GEO

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior I

Project description:Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior I

| PRJNA472567 | ENA

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior II

Project description:Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior II

| PRJNA472569 | ENA

Reducing astrocyte calcium signaling in vivo alters striatal microcircuits and causes repetitive behavior

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-05-09 | GSE114757 | GEO

Reducing Astrocyte Calcium Signaling In Vivo Alters Striatal Microcircuits and Causes Repetitive Behavior.

Project description:Astrocytes tile the central nervous system, but their functions in neural microcircuits in vivo and their roles in mammalian behavior remain incompletely defined. We used two-photon laser scanning microscopy, electrophysiology, MINIscopes, RNA-seq, and a genetic approach to explore the effects of reduced striatal astrocyte Ca2+ signaling in vivo. In wild-type mice, reducing striatal astrocyte Ca2+-dependent signaling increased repetitive self-grooming behaviors by altering medium spiny neuron (MSN) activity. The mechanism involved astrocyte-mediated neuromodulation facilitated by ambient GABA and was corrected by blocking astrocyte GABA transporter 3 (GAT-3). Furthermore, in a mouse model of Huntington's disease, dysregulation of GABA and astrocyte Ca2+ signaling accompanied excessive self-grooming, which was relieved by blocking GAT-3. Assessments with RNA-seq revealed astrocyte genes and pathways regulated by Ca2+ signaling in a cell-autonomous and non-cell-autonomous manner, including Rab11a, a regulator of GAT-3 functional expression. Thus, striatal astrocytes contribute to neuromodulation controlling mouse obsessive-compulsive-like behavior.

| S-EPMC6450394 | biostudies-literature

Striatal and hippocampal astrocyte proteomes

Project description:We quantitavely compared striatal and hippocampal astrocyte proteomes using stable-isotopic dimethyl labeling.

2017-07-10 | PXD005852 | Pride

Inflammatory mediators alter astrocyte genomic profiles and G-protein receptor evoked calcium signaling

Project description:Inflammation features in diverse central nervous system disorders such as stroke, trauma, neurodegeneration, infection and autoimmunity. To better understand how inflammatory mediators may alter astrocyte functions, we examined the effects of transforming growth factor-Î²1 (TGF-Î²1), lipopolysaccharide (LPS) and interferon-gamma (IFNÎ³) on purified, murine, primary cortical astrocyte cultures. We used microarrays to conduct whole genome expression profiling, and measured calcium signaling, which is implicated in mediating dynamic astrocyte functions. Combinatorial exposure to TGF-Î²1, LPS and IFNÎ³ significantly modulated astrocyte expression of over 6,800 genes and resulted in both additive and synergistic changes compared with individual stimuli alone. Bioinformatic analysis revealed that combinatorial treatment significantly and markedly up regulated molecular networks and pathways associated with immune signaling and with regulation of cell compromise, death, growth and proliferation. These findings provide databases of astrocyte transcriptome changes elicited by the inflammatory stimuli, TGF-Î²1, LPS and IFNÎ³ alone and in combination, and show that these stimuli up regulate astrocyte molecular networks associated with immune- and injury-related functions and significantly alter astrocyte calcium signaling evoked by multiple GPCR. We used microarrays to examine the effects of transforming growth factor-Î²1 (TGF-Î²1), lipopolysaccharide (LPS) and interferon-gamma (IFNÎ³) on purified, murine, primary cortical astrocyte cultures.

2012-10-18 | E-GEOD-36089 | biostudies-arrayexpress

Astrocyte and neuron subcompartment proteomes reveal distinct cellular and molecular mechanisms of OCD

Project description:Astrocytes and neurons coexist and interact in the CNS1,2. Given that many signaling and pathological events are protein-driven, identifying astrocyte and neuron proteomes is essential for elucidating the complex protein networks that dictate their respective contributions to physiology and disease. Here, we used cell- and subcompartment-specific proximity-dependent biotinylation3 to study the proteomes of striatal astrocytes and medium spiny neurons (MSNs) in vivo. We evaluated cytosolic and plasma membrane compartments for astrocytes and MSNs, revealing how these cells differ at the protein level and in their core signaling machinery. We assessed subcellular compartments of astrocytes including end feet and processes to reveal the molecular basis of essential astrocyte signaling and homeostatic functions. Unexpectedly, SAPAP3 proteins (gene; Dlgap3) associated with obsessive compulsive disorder (OCD) and repetitive behaviors4-11 were detected at equivalent levels in striatal astrocyte and MSN plasma membrane and cytosolic compartments. Astrocytic expression was confirmed by RNA-seq, fluorescence in situ hybridization and immunohistochemistry. Furthermore, genetic rescue experiments combined with behavioral analyses and proteomics in a mouse model4 of OCD lacking SAPAP3 revealed contributions of SAPAP3 in astrocytes and MSNs to repetitive and anxiety-related OCD behaviors. Our data define how astrocytes and neurons differ at the protein level and in their major signaling pathways, how astrocyte proteomes vary between physiological subcompartments, and how specific astrocyte and neuronal molecular mechanisms contribute to a psychiatric disease. Targeting both astrocytes and neurons together is likely to be therapeutically effective in complex CNS disorders.

2023-01-13 | PXD029257 | Pride

Striatal transcriptome changes linked to drug-induced repetitive behaviors

Project description:Striatal transcriptome changes linked to drug-induced repetitive behaviors

| PRJNA663329 | ENA