Gene expression changes induced by noradrenaline stimulation in cultured mouse cortical astrocytes
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE325814 | GEO | 2026/03/31
REPOSITORIES: GEO
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Project description:Gene expression changes induced by noradrenaline stimulation in cultured mouse cortical astrocytes
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Project description:Astrocytes are essential regulators of neuronal function and brain homeostasis. While chemogenetic strategies, such as DREADD (Designer Receptors Exclusively Activated by Designer Drugs), are frequently employed to specifically modulate astrocyte activity, the molecular mechanisms accompanying their activation remain incompletely understood. Here, we characterized the transcriptional responses of cultured cortical astrocytes to DREADD stimulation. These findings provide a molecular framework for interpreting astrocytic DREADD manipulations.
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Project description:Here, we extensively characterize noradrenaline (NA) mediated transcriptomic response during acute stress in the mouse hippocampus. Combining for the first time bulk mRNA-sequencing and selective pharmacological manipulations of the NA system. We show that the NA mediates robust stress associated transcriptomic alterations across the dorsal and ventral hippocampus via β-adrenergic receptors
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Project description:Oligodendrocyte precusor cells (OPCs) exhibit near membrane calcium transients that can be enhacned by norepinephrine-mediated activation of alpha1A adrenergic receptors in vivo. In order to determine if norepinephrine directly modulates OPC behaviors, we performed an unbiased, transcriptomic-based assessment of biological processes altered in OPCs after activation of alpha1 adrenergic receptors
2023-06-26 | GSE226635 | GEO
Project description:Cultures of dissociated cortical neurons represent a powerful trade-off between more realistic experimental models and abstract modeling approaches, allowing to investigate mechanisms of synchronized activity generation. These networks spontaneously alternate periods of high activity (i.e. network bursts) with periods of quiescence in a dynamic state which recalls the fluctuation of in vivo UP and DOWN states. Network bursts can also be elicited by external stimulation and their spatial propagation patterns tracked by means of multi-channel micro-electrode arrays. In this study, we used rat cortical cultures coupled to micro-electrode arrays to investigate the similarity between spontaneous and evoked activity patterns. We performed experiments by applying electrical stimulation to different network locations and demonstrated that the rank orders of electrodes during evoked and spontaneous events are remarkably similar independently from the stimulation source. We linked this result to the capability of stimulation to evoke firing in highly active and "leader" sites of the network, reliably and rapidly recruited within both spontaneous and evoked bursts. Our study provides the first evidence that spontaneous and evoked activity similarity is reliably observed also in dissociated cortical networks.
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Project description:In central nervous system, glycine receptor (GlyR) is mostly expressed in the spinal cord and brainstem, but glycinergic transmission related elements have also been identified in the brain. Astrocytes are active elements at the tripartite synapse, being responsible for the maintenance of brain homeostasis and for the fine-tuning of synaptic activity. These cells communicate, spontaneously or in response to a stimulus, by elevations in their cytosolic calcium (calcium transients, Ca2+T) that can be propagated to other cells. How these Ca2+T are negatively modulated is yet poorly understood. In this work, we evaluated GlyR expression and its role on calcium signaling modulation in rat brain astrocytes. We first proved that GlyR, predominantly subunits α2 and β, was expressed in brain astrocytes and its localization was confirmed in the cytoplasm and astrocytic processes by immunohistochemistry assays. Calcium imaging experiments in cultured astrocytes showed that glycine (500 μM), a GlyR agonist, caused a concentration-dependent reduction in ATP-induced Ca2+T, an effect abolished by the GlyR antagonist, strychnine (0.8 μM), as well as by nocodazole (1 μM), known to impair GlyR anchorage to the plasma membrane. This effect was mimicked by activation of GABAAR, another Cl--permeable channel. In summary, we demonstrated that GlyR activation in astrocytes mediates an inhibitory effect upon ATP induced Ca2+T, which most probably involves changes in membrane permeability to Cl- and requires GlyR anchorage at the plasma membrane. GlyR in astrocytes may thus be part of a mechanism to modulate astrocyte-to-neuron communication.
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Project description:Noradrenaline regulates cold-stimulated adipocyte thermogenesis. Aside from cAMP signaling downstream of β-adrenergic receptor (βAR) activation, how noradrenaline promotes thermogenic output is still not fully understood. Here, we show that coordinated α1-adrenergic receptor (α1AR) and β3AR signaling induces the expression of thermogenic genes of the futile creatine cycle, and that EBFs, ERRs, and PGC1α are required for this response in vivo. Noradrenaline triggers physical and functional coupling between the α1AR subtype (ADRA1A) to Gαq to promote adipocyte thermogenesis in a manner that is dependent on the effector proteins of the futile creatine cycle, creatine kinase b (CKB) and tissue-nonspecific alkaline phosphatase (TNAP). Combined Gαq and Gαs signaling selectively in adipocytes promotes a continual rise in whole-body energy expenditure, and CKB is required for this effect. Thus, the ADRA1A-Gαq-futile creatine cycle axis is a key regulator of facultative and adaptive thermogenesis.
2022-09-08 | GSE207340 | GEO
Project description:Noradrenaline regulates cold-stimulated adipocyte thermogenesis. Aside from cAMP signaling downstream of β-adrenergic receptor (βAR) activation, how noradrenaline promotes thermogenic output is still not fully understood. Here, we show that coordinated α1-adrenergic receptor (α1AR) and β3AR signaling induces the expression of thermogenic genes of the futile creatine cycle, and that EBFs, ERRs, and PGC1α are required for this response in vivo. Noradrenaline triggers physical and functional coupling between the α1AR subtype (ADRA1A) to Gαq to promote adipocyte thermogenesis in a manner that is dependent on the effector proteins of the futile creatine cycle, creatine kinase b (CKB) and tissue-nonspecific alkaline phosphatase (TNAP). Combined Gαq and Gαs signaling selectively in adipocytes promotes a continual rise in whole-body energy expenditure, and CKB is required for this effect. Thus, the ADRA1A-Gαq-futile creatine cycle axis is a key regulator of facultative and adaptive thermogenesis.
2022-09-08 | GSE207341 | GEO
Project description:Astrocytes play essential roles in the developing nervous system, including supporting synapse function. These astrocyte support functions emerge coincident with brain maturation and may be tailored in a region-specific manner. For example, gray matter astrocytes have elaborate synapse-associated processes and are morphologically and molecularly distinct from white-matter astrocytes. This raises the question of whether there are unique environmental cues that promote gray matter astrocyte identity and synaptogenic function. We previously identified adrenergic receptors as preferentially enriched in developing gray versus white matter astrocytes, suggesting that noradrenergic signaling could be a cue that promotes the functional maturation of gray matter astrocytes. We first characterized noradrenergic projections during postnatal brain development in mouse and human, finding that process density was higher in the gray matter and increased concurrently with astrocyte maturation. RNA-sequencing revealed that astrocytes in both species expressed ɑ and β adrenergic receptors. We found that stimulation of β adrenergic receptors increased primary branching of rodent astrocytes in vitro. Conversely, astrocyte-conditional knockout of the β1 adrenergic receptor reduced the size of gray matter astrocytes, and led to dysregulated sensorimotor integration in female mice. These studies suggest that adrenergic signaling to developing astrocytes impacts their morphology and has implications for adult behavior, particularly in female animals. More broadly, they demonstrate a mechanism through which environmental cues impact astrocyte development. Given the key roles of norepinephrine in brain states such as arousal, stress, and learning, these findings could prompt further inquiry into how developmental stressors impact astrocyte development and adult brain function.
2023-12-27 | GSE235840 | GEO