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Bioenergetic control of synaptic plasticity by astrocytes during acute stress

ABSTRACT: Aldh1l1CreERT2-RiboTag mice were used to purify and sequence astrocyte actively translated mRNAs from acute stress mouse models (20 minute forced swim) and non stressed controls.

ORGANISM(S): Mus musculus

PROVIDER: GSE126172 | GEO | 2020/03/13

REPOSITORIES: GEO

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Neural circuit-specialized astrocytes: genomic, proteomic, morphological and functional evidence

Project description:The Khakh laboratory used Aldh1l1-Cre/ERT2 transgenic mouse line crossed with RiboTag mice to sequence actively translated mRNAs and compare striatal and hippocampal astrocyte transcriptomes from adults.

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New transgenic mouse lines for selectively targeting astrocytes and for studying calcium signals in astrocyte processes in situ and in vivo

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The proteome and phosphoproteome of acute stress in the mouse hippocampus (addendum phosphoproteomics males vs females)

Project description:This is an addendum for PXD024829 that was produced in the revision process. These additional data investigate the effect of forced swim stress on the phosphoproteome of male vs female mice immediately after stress exposure

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RiboTag analysis of actively translated mRNAs in Sertoli and Leydig cells in vivo

Project description:Analysis of Sertoli and Leydig cell “translatome” utilizing an in vivo ribosome tagging strategy (RiboTag) that allows a detailed and physiologically relevant characterization of the polysome-associated mRNAs in vivo. Although progress has been made in the identification of specific transcripts that are translated in Sertoli and Leydig cells and their response to hormones, efforts to expand these studies have been restricted by technical hurdles. Our analysis identified all previously characterized Leydig and Sertoli cell-specific markers and identified in a comprehensive manner novel markers of Leydig and Sertoli cells; the translational response of these two cell types to gonadotropins or testosterone was also investigated. Leydig cell-specific (Cyp17iCre: RiboTag) and Sertoli cell-specific (AMH-Cre: RiboTag) RiboTag mice were obtained by crossing RiboTag homozygous mice with Cyp17iCre or AMH-Cre mice. For in vivo LH treatment experiments, mice were injected with the GnRH antagonist acyline for 4 days before a single injection of purified human LH. After treatment, testes were homogenized and polysomes were immunoprecipitated by utilizing an anti-HA antibody. RNA was extracted, labelled, and hybridized to Mouse Gene ST 1.0 arrays.

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Project description:We used microarrays to identify the gene with altered expression in the hippocampus of depression mouse model with forced swim stress campared to control mice .

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Project description:We show that infant trauma, as modeled by infant paired odor-shock conditioning, results in later life depressive-like behavior that can be modulated by learned infant cues (i.e., odor previously paired with shock). We have previously shown that this infant attachment odor learning paradigm results in the creation of a new artificial maternal odor that is able to control pup behavior and retain its value throughout development. Here, we assess the mechanism by which this artificial maternal odor is able to rescue depressive-like behavior and show that this anti-depressant like effect results in glucocorticoid and serotonin (5-HT) related changes in amygdala gene expression and is dependent on amygdala 5-HT. Furthermore, increasing amygdala 5-HT and blocking corticosterone (CORT) in the absence of odor mimics the adult rescue effects elicited by the artificial maternal odor, suggesting a mechanism by which odor presentation exerts its repair effects. There are three experimental groups: 1: pups with no infant shock and the adult forced swim test (FST)with no odor; 2. pups with infant odor-shock pairing and the adult forced swim test (FST) with no odor; 3. pups with infant odor-shock pairing and adult forced swim test with infant odor.

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Bioenergetic control of synaptic plasticity by astrocytes during acute stress

Project description:Bioenergetic control of synaptic plasticity by astrocytes during acute stress

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