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Journal articles on the topic 'Astrocytes'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Nett, Wolfgang J., Scott H. Oloff, and Ken D. McCarthy. "Hippocampal Astrocytes In Situ Exhibit Calcium Oscillations That Occur Independent of Neuronal Activity." Journal of Neurophysiology 87, no. 1 (2002): 528–37. http://dx.doi.org/10.1152/jn.00268.2001.

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Results presented in this study indicate that a large subpopulation (∼65%) of hippocampal astrocytes in situ exhibit calcium oscillations in the absence of neuronal activity. Further, the spontaneous oscillations observed within individual hippocampal astrocytes generally developed asynchronously throughout the astrocyte's fine processes and occasionally spread through a portion of that astrocyte as a calcium wave but do not appear to spread among astrocytes as an intercellular calcium wave. Bath application of cyclopiazonic acid and injection of individual astrocytes with heparin blocked astr

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2

Huang, Mi, Yixing Du, Conrad Kiyoshi, et al. "Syncytial Isopotentiality: An Electrical Feature of Spinal Cord Astrocyte Networks." Neuroglia 1, no. 1 (2018): 271–79. http://dx.doi.org/10.3390/neuroglia1010018.

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Due to strong electrical coupling, syncytial isopotentiality emerges as a physiological mechanism that coordinates astrocytes into a highly efficient system in brain homeostasis. Although this electrophysiological phenomenon has now been observed in astrocyte networks established by different astrocyte subtypes, the spinal cord remains a brain region that is still unexplored. In ALDH1L1-eGFP transgenic mice, astrocytes can be visualized by confocal microscopy and the spinal cord astrocytes in grey matter are organized in a distinctive pattern. Namely, each astrocyte resides with more directly

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Domingos, Cátia, Franziska E. Müller, Stefan Passlick, et al. "Induced Remodelling of Astrocytes In Vitro and In Vivo by Manipulation of Astrocytic RhoA Activity." Cells 12, no. 2 (2023): 331. http://dx.doi.org/10.3390/cells12020331.

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Structural changes of astrocytes and their perisynaptic processes occur in response to various physiological and pathophysiological stimuli. They are thought to profoundly affect synaptic signalling and neuron-astrocyte communication. Understanding the causal relationship between astrocyte morphology changes and their functional consequences requires experimental tools to selectively manipulate astrocyte morphology. Previous studies indicate that RhoA-related signalling can play a major role in controlling astrocyte morphology, but the direct effect of increased RhoA activity has not been docu

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Amuti, T., I. Ouko, S. Mukonjia, et al. "Role of heterogeneous astrocyte receptor expression in determining astrocytic response to neuronal disorders." Anatomy Journal of Africa 7, no. 1 (2018): 1169–74. http://dx.doi.org/10.4314/aja.v7i1.169490.

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Following neuronal disorders, astrocytes carry out either neuroprotection or neurodegeneration. Previous authors suggest that favoring of neurodegeneration or neuroprotection by astrocytes can be due to many factors such as the influence of cytokines following their binding on their receptors on astrocytes. These receptors have however been shown to be region specific and heterogeneous. Further, research exploiting their role and influence in determining astrocytic response remains partly elucidated. A review of previous and ongoing research on these receptors would be helpful in the disclosur

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Wolfes, Anne C., Saheeb Ahmed, Ankit Awasthi, et al. "A novel method for culturing stellate astrocytes reveals spatially distinct Ca2+ signaling and vesicle recycling in astrocytic processes." Journal of General Physiology 149, no. 1 (2016): 149–70. http://dx.doi.org/10.1085/jgp.201611607.

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Interactions between astrocytes and neurons rely on the release and uptake of glial and neuronal molecules. But whether astrocytic vesicles exist and exocytose in a regulated or constitutive fashion is under debate. The majority of studies have relied on indirect methods or on astrocyte cultures that do not resemble stellate astrocytes found in vivo. Here, to investigate vesicle-associated proteins and exocytosis in stellate astrocytes specifically, we developed a simple, fast, and economical method for growing stellate astrocyte monocultures. This method is superior to other monocultures in t

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Escalada, Paula, Amaia Ezkurdia, María Javier Ramírez, and Maite Solas. "Essential Role of Astrocytes in Learning and Memory." International Journal of Molecular Sciences 25, no. 3 (2024): 1899. http://dx.doi.org/10.3390/ijms25031899.

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One of the most biologically relevant functions of astrocytes within the CNS is the regulation of synaptic transmission, i.e., the physiological basis for information transmission between neurons. Changes in the strength of synaptic connections are indeed thought to be the cellular basis of learning and memory. Importantly, astrocytes have been demonstrated to tightly regulate these processes via the release of several gliotransmitters linked to astrocytic calcium activity as well as astrocyte–neuron metabolic coupling. Therefore, astrocytes seem to be integrators of and actors upon learning-

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Noeker, Jacob, Carmen Nanclares, Alfonso Araque, and Andrés Baraibar. "Astrocyte-neuron signaling in aging." Ageing & Longevity, no. 2. 2025 (February 27, 2025): 136–43. https://doi.org/10.47855/jal9020-2025-2-5.

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Rapid increases in the aging population present a critical challenge to global societies, with a major concern being cognitive decline and brain aging. While neuroscientific research has traditionally focused on neurons, the role of astrocytes in aging is of recent interest but remains underexplored. Astrocytes, the homeostatic cells on the central nervous system, play essential roles in synaptic regulation, neurotransmitter clearance, neuronal support, and homeostasis. Recent studies indicate that astrocytes undergo significant morphological and functional changes during aging, affecting calc

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Nassar, Ajmal, Triveni Kodi, Sairaj Satarker, et al. "Astrocytic MicroRNAs and Transcription Factors in Alzheimer’s Disease and Therapeutic Interventions." Cells 11, no. 24 (2022): 4111. http://dx.doi.org/10.3390/cells11244111.

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Astrocytes are important for maintaining cholesterol metabolism, glutamate uptake, and neurotransmission. Indeed, inflammatory processes and neurodegeneration contribute to the altered morphology, gene expression, and function of astrocytes. Astrocytes, in collaboration with numerous microRNAs, regulate brain cholesterol levels as well as glutamatergic and inflammatory signaling, all of which contribute to general brain homeostasis. Neural electrical activity, synaptic plasticity processes, learning, and memory are dependent on the astrocyte–neuron crosstalk. Here, we review the involvement of

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Emerson, Jacen, Thomas Delgado, Peter Girardi, and Gail V. W. Johnson. "Deletion of Transglutaminase 2 from Mouse Astrocytes Significantly Improves Their Ability to Promote Neurite Outgrowth on an Inhibitory Matrix." International Journal of Molecular Sciences 24, no. 7 (2023): 6058. http://dx.doi.org/10.3390/ijms24076058.

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Astrocytes are the primary support cells of the central nervous system (CNS) that help maintain the energetic requirements and homeostatic environment of neurons. CNS injury causes astrocytes to take on reactive phenotypes with an altered overall function that can range from supportive to harmful for recovering neurons. The characterization of reactive astrocyte populations is a rapidly developing field, and the underlying factors and signaling pathways governing which type of reactive phenotype that astrocytes take on are poorly understood. Our previous studies suggest that transglutaminase 2

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Koyama, Yutaka. "Endothelin ETB Receptor-Mediated Astrocytic Activation: Pathological Roles in Brain Disorders." International Journal of Molecular Sciences 22, no. 9 (2021): 4333. http://dx.doi.org/10.3390/ijms22094333.

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In brain disorders, reactive astrocytes, which are characterized by hypertrophy of the cell body and proliferative properties, are commonly observed. As reactive astrocytes are involved in the pathogenesis of several brain disorders, the control of astrocytic function has been proposed as a therapeutic strategy, and target molecules to effectively control astrocytic functions have been investigated. The production of brain endothelin-1 (ET-1), which increases in brain disorders, is involved in the pathophysiological response of the nervous system. Endothelin B (ETB) receptors are highly expres

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11

Inyushin, M. Y., A. Huertas, Y. V. Kucheryavykh, et al. "L-DOPA Uptake in Astrocytic Endfeet Enwrapping Blood Vessels in Rat Brain." Parkinson's Disease 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/321406.

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Astrocyte endfeet surround brain blood vessels and can play a role in the delivery of therapeutic drugs for Parkinson’s disease. However, there is no previous evidence of the presence of LAT transporter forL-DOPA in brain astrocytes except in culture. Using systemicL-DOPA administration and a combination of patch clamp, histochemistry and confocal microscopy we found thatL-DOPA is accumulated mainly in astrocyte cell bodies, astrocytic endfeet surrounding blood vessels, and pericytes. In brain slices: (1) astrocytes were exposed to ASP+, a fluorescent monoamine analog of MPP+; (2) ASP+taken up

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Skowrońska, Katarzyna, Marta Obara-Michlewska, Magdalena Zielińska, and Jan Albrecht. "NMDA Receptors in Astrocytes: In Search for Roles in Neurotransmission and Astrocytic Homeostasis." International Journal of Molecular Sciences 20, no. 2 (2019): 309. http://dx.doi.org/10.3390/ijms20020309.

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Studies of the last two decades have demonstrated the presence in astrocytic cell membranes of N-methyl-d-aspartate (NMDA) receptors (NMDARs), albeit their apparently low abundance makes demonstration of their presence and function more difficult than of other glutamate (Glu) receptor classes residing in astrocytes. Activation of astrocytic NMDARs directly in brain slices and in acutely isolated or cultured astrocytes evokes intracellular calcium increase, by mutually unexclusive ionotropic and metabotropic mechanisms. However, other than one report on the contribution of astrocyte-located NMD

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Rouach, Nathalie, Jacques Glowinski, and Christian Giaume. "Activity-Dependent Neuronal Control of Gap-Junctional Communication in Astrocytes." Journal of Cell Biology 149, no. 7 (2000): 1513–26. http://dx.doi.org/10.1083/jcb.149.7.1513.

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A typical feature of astrocytes is their high degree of intercellular communication through gap junction channels. Using different models of astrocyte cultures and astrocyte/neuron cocultures, we have demonstrated that neurons upregulate gap-junctional communication and the expression of connexin 43 (Cx43) in astrocytes. The propagation of intercellular calcium waves triggered in astrocytes by mechanical stimulation was also increased in cocultures. This facilitation depends on the age and number of neurons, indicating that the state of neuronal differentiation and neuron density constitute tw

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Yang, Sijie (Shirley), Svetlana Simtchouk, Julien Gibon, and Andis Klegeris. "Regulation of the phagocytic activity of astrocytes by neuroimmune mediators endogenous to the central nervous system." PLOS ONE 18, no. 7 (2023): e0289169. http://dx.doi.org/10.1371/journal.pone.0289169.

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The phagocytic activity of glial cells is essential for maintaining normal brain activity, and its dysfunction may contribute to the central nervous system (CNS) pathologies, including neurodegenerative diseases. Phagocytic activity is one of the well-established neuroimmune functions of microglia. Although emerging evidence indicates that astrocytes can also function as CNS phagocytes in humans and rodents, limited information is available about the molecular mechanism regulating this function. To address this knowledge gap, we studied modulation of the phagocytic activity of human U118 MG as

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Devaraju, Prakash, Min-Yu Sun, Timothy L. Myers, Kelli Lauderdale, and Todd A. Fiacco. "Astrocytic group I mGluR-dependent potentiation of astrocytic glutamate and potassium uptake." Journal of Neurophysiology 109, no. 9 (2013): 2404–14. http://dx.doi.org/10.1152/jn.00517.2012.

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One of the most important functions of astrocytes is removal of glutamate released during synaptic transmission. Surprisingly, the mechanisms by which astrocyte glutamate uptake is acutely modulated remain to be clarified. Astrocytes express metabotropic glutamate receptors (mGluRs) and other G protein-coupled receptors (GPCRs), which are activated during neuronal activity. Here, we test the hypothesis that astrocytic group I mGluRs acutely regulate glutamate uptake by astrocytes in situ. This hypothesis was tested in acute mouse hippocampal slices. Activation of astrocytic mGluRs, using a tet

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16

Feng, Shuai, Juanji Li, Tingting Liu, et al. "Overexpression of low-density lipoprotein receptor prevents neurotoxic polarization of astrocytes via inhibiting NLRP3 inflammasome activation in experimental ischemic stroke." Neural Regeneration Research 20, no. 2 (2024): 491–502. http://dx.doi.org/10.4103/nrr.nrr-d-23-01263.

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JOURNAL/nrgr/04.03/01300535-202502000-00027/figure1/v/2024-06-06T062529Z/r/image-tiff Neurotoxic astrocytes are a promising therapeutic target for the attenuation of cerebral ischemia/reperfusion injury. Low-density lipoprotein receptor, a classic cholesterol regulatory receptor, has been found to inhibit NLR family pyrin domain containing protein 3 (NLRP3) inflammasome activation in neurons following ischemic stroke and to suppress the activation of microglia and astrocytes in individuals with Alzheimer’s disease. However, little is known about the effects of low-density lipoprotein receptor

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SUL, JAI-YOON, GEORGE OROSZ, RICHARD S. GIVENS, and PHILIP G. HAYDON. "Astrocytic Connectivity in the Hippocampus." Neuron Glia Biology 1, no. 1 (2004): 3–11. http://dx.doi.org/10.1017/s1740925x04000031.

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Little is known about the functional connectivity between astrocytes in the CNS. To explore this issue we photo-released glutamate onto a single astrocyte in murine hippocampal slices and imaged calcium responses. Photo-release of glutamate causes a metabotropic glutamate receptor (mGluR)-dependent increase in internal calcium in the stimulated astrocyte and delayed calcium elevations in neighboring cells. The delayed elevation in calcium was not caused by either neuronal activity following synaptic transmission or by glutamate released from astrocytes. However, it was reduced by flufenamic ac

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18

Birck, Cindy, Aurélien Ginolhac, Maria Angeliki S. Pavlou, Alessandro Michelucci, Paul Heuschling та Luc Grandbarbe. "NF-κB and TNF Affect the Astrocytic Differentiation from Neural Stem Cells". Cells 10, № 4 (2021): 840. http://dx.doi.org/10.3390/cells10040840.

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The NF-κB signaling pathway is crucial during development and inflammatory processes. We have previously shown that NF-κB activation induces dedifferentiation of astrocytes into neural progenitor cells (NPCs). Here, we provide evidence that the NF-κB pathway plays also a fundamental role during the differentiation of NPCs into astrocytes. First, we show that the NF-κB pathway is essential to initiate astrocytic differentiation as its early inhibition induces NPC apoptosis and impedes their differentiation. Second, we demonstrate that persistent NF-κB activation affects NPC-derived astrocyte di

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19

Peteri, Ulla-Kaisa, Juho Pitkonen, Kagistia Hana Utami, et al. "Generation of the Human Pluripotent Stem-Cell-Derived Astrocyte Model with Forebrain Identity." Brain Sciences 11, no. 2 (2021): 209. http://dx.doi.org/10.3390/brainsci11020209.

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Astrocytes form functionally and morphologically distinct populations of cells with brain-region-specific properties. Human pluripotent stem cells (hPSCs) offer possibilities to generate astroglia for studies investigating mechanisms governing the emergence of astrocytic diversity. We established a method to generate human astrocytes from hPSCs with forebrain patterning and final specification with ciliary neurotrophic factor (CNTF). Transcriptome profiling and gene enrichment analysis monitored the sequential expression of genes determining astrocyte differentiation and confirmed activation o

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Zhang, Zengli, Zhi Ma, Wangyuan Zou, et al. "The Appropriate Marker for Astrocytes: Comparing the Distribution and Expression of Three Astrocytic Markers in Different Mouse Cerebral Regions." BioMed Research International 2019 (June 24, 2019): 1–15. http://dx.doi.org/10.1155/2019/9605265.

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Astrocytes possess different morphological characteristics depending on the cerebral region in which they are found. However, none of the current astrocytic markers can label all subpopulations successfully. Thus, identifying the appropriate marker for a specific scientific investigation is critical. Here, we compared the distribution and protein expression of three astrocyte markers: NDRG2, GFAP, and S100β, in the cortex, hippocampus, and thalamus. NDRG2- and S100β-positive astrocytes were distributed more uniformly than GFAP-positive astrocytes throughout the whole cerebrum. NDRG2 and S100βi

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Barnett, Daniel, Kirsten Bohmbach, Valentin Grelot, et al. "Astrocytes as Drivers and Disruptors of Behavior: New Advances in Basic Mechanisms and Therapeutic Targeting." Journal of Neuroscience 43, no. 45 (2023): 7463–71. http://dx.doi.org/10.1523/jneurosci.1376-23.2023.

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Astrocytes are emerging as key regulators of cognitive function and behavior. This review highlights some of the latest advances in the understanding of astrocyte roles in different behavioral domains across lifespan and in disease. We address specific molecular and circuit mechanisms by which astrocytes modulate behavior, discuss their functional diversity and versatility, and highlight emerging astrocyte-targeted treatment strategies that might alleviate behavioral and cognitive dysfunction in pathologic conditions. Converging evidence across different model systems and manipulations is reve

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Zhou, Zhiwen, Kazuki Okamoto, Junya Onodera, et al. "Astrocytic cAMP modulates memory via synaptic plasticity." Proceedings of the National Academy of Sciences 118, no. 3 (2021): e2016584118. http://dx.doi.org/10.1073/pnas.2016584118.

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Astrocytes play a key role in brain homeostasis and functions such as memory. Specifically, astrocytes express multiple receptors that transduce signals via the second messenger cAMP. However, the involvement of astrocytic cAMP in animal behavior and the underlying glial–neuronal interactions remains largely unknown. Here, we show that an increase in astrocytic cAMP is sufficient to induce synaptic plasticity and modulate memory. We developed a method to increase astrocytic cAMP levels in vivo using photoactivated adenylyl cyclase and found that increased cAMP in hippocampal astrocytes at diff

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Cirillo, Giovanni, Daniele De Luca, and Michele Papa. "Calcium Imaging of Living Astrocytes in the Mouse Spinal Cord following Sensory Stimulation." Neural Plasticity 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/425818.

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Astrocytic Ca2+dynamics have been extensively studied inex vivomodels; however, the recent development of two-photon microscopy and astrocyte-specific labeling has allowed the study of Ca2+signaling in living central nervous system. Ca2+waves in astrocytes have been described in cultured cells and slice preparations, but evidence for astrocytic activation during sensory activity is lacking. There are currently few methods to image living spinal cord: breathing and heart-beating artifacts have impeded the widespread application of this technique. We here imaged the living spinal cord by two-pho

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Saas, Philippe, José Boucraut, Anne-Lise Quiquerez, et al. "CD95 (Fas/Apo-1) as a Receptor Governing Astrocyte Apoptotic or Inflammatory Responses: A Key Role in Brain Inflammation?" Journal of Immunology 162, no. 4 (1999): 2326–33. http://dx.doi.org/10.4049/jimmunol.162.4.2326.

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Abstract Astrocytes are a major cellular component of the brain that are capable of intense proliferation and metabolic activity during diverse inflammatory brain diseases (such as multiple sclerosis, Alzheimer’s dementia, tumor, HIV encephalitis, or prion disease). In this biological process, called reactive gliosis, astrocyte apoptosis is frequently observed and could be an important mechanism of regulation. However, the factors responsible for apoptosis in human astrocytes are poorly defined. Here, we report that short term cultured astrocytes derived from different brain regions express si

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Rosa, Juao-Guilherme, Katherine Hamel, Carrie Sheeler, et al. "Spatial and Temporal Diversity of Astrocyte Phenotypes in Spinocerebellar Ataxia Type 1 Mice." Cells 11, no. 20 (2022): 3323. http://dx.doi.org/10.3390/cells11203323.

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While astrocyte heterogeneity is an important feature of the healthy brain, less is understood about spatiotemporal heterogeneity of astrocytes in brain disease. Spinocerebellar ataxia type 1 (SCA1) is a progressive neurodegenerative disease caused by a CAG repeat expansion in the gene Ataxin1 (ATXN1). We characterized astrocytes across disease progression in the four clinically relevant brain regions, cerebellum, brainstem, hippocampus, and motor cortex, of Atxn1154Q/2Q mice, a knock-in mouse model of SCA1. We found brain region-specific changes in astrocyte density and GFAP expression and ar

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Pillai, Anup Gopalakrishna, and Suhita Nadkarni. "Amyloid pathology disrupts gliotransmitter release in astrocytes." PLOS Computational Biology 18, no. 8 (2022): e1010334. http://dx.doi.org/10.1371/journal.pcbi.1010334.

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Accumulation of amyloid-beta (Aβ) is associated with synaptic dysfunction and destabilization of astrocytic calcium homeostasis. A growing body of evidence support astrocytes as active modulators of synaptic transmission via calcium-mediated gliotransmission. However, the details of mechanisms linking Aβ signaling, astrocytic calcium dynamics, and gliotransmission are not known. We developed a biophysical model that describes calcium signaling and the ensuing gliotransmitter release from a single astrocytic process when stimulated by glutamate release from hippocampal neurons. The model accura

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Tatomir, Alexandru, Dallas Boodhoo, Vinh Nguyen, et al. "RGC-32 regulates astrocyte differentiation during experimental autoimmune encephalomyelitis." Journal of Immunology 204, no. 1_Supplement (2020): 64.9. http://dx.doi.org/10.4049/jimmunol.204.supp.64.9.

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Abstract Astrocytes are increasingly recognized as critical contributors to multiple sclerosis pathogenesis. We have previously shown that lack of response gene to complement 32 (RGC-32) alters astrocyte morphology in spinal cords during experimental autoimmune encephalomyelitis (EAE), suggesting a role for RGC-32 in astrocyte differentiation. In addition, we found that RGC-32 regulates TGF-β-induced extracellular matrix production and growth factors expression. We investigated if the lack of RGC-32 alters the expression of the glial fibrillary acidic protein (GFAP) and of astrocytes progenito

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Michinaga, Shotaro, and Yutaka Koyama. "Pathophysiological Responses and Roles of Astrocytes in Traumatic Brain Injury." International Journal of Molecular Sciences 22, no. 12 (2021): 6418. http://dx.doi.org/10.3390/ijms22126418.

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Traumatic brain injury (TBI) is immediate damage caused by a blow to the head resulting from traffic accidents, falls, and sporting activity, which causes death or serious disabilities in survivors. TBI induces multiple secondary injuries, including neuroinflammation, disruption of the blood–brain barrier (BBB), and brain edema. Despite these emergent conditions, current therapies for TBI are limited or insufficient in some cases. Although several candidate drugs exerted beneficial effects in TBI animal models, most of them failed to show significant effects in clinical trials. Multiple studie

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Cho, Sukhee, Allie K. Muthukumar, Tobias Stork, Jaeda C. Coutinho-Budd, and Marc R. Freeman. "Focal adhesion molecules regulate astrocyte morphology and glutamate transporters to suppress seizure-like behavior." Proceedings of the National Academy of Sciences 115, no. 44 (2018): 11316–21. http://dx.doi.org/10.1073/pnas.1800830115.

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Astrocytes are important regulators of neural circuit function and behavior in the healthy and diseased nervous system. We screened for molecules in Drosophila astrocytes that modulate neuronal hyperexcitability and identified multiple components of focal adhesion complexes (FAs). Depletion of astrocytic Tensin, β-integrin, Talin, focal adhesion kinase (FAK), or matrix metalloproteinase 1 (Mmp1), resulted in enhanced behavioral recovery from genetic or pharmacologically induced seizure. Overexpression of Mmp1, predicted to activate FA signaling, led to a reciprocal enhancement of seizure sever

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Slavi, Nefeli, Abduqodir H. Toychiev, Stylianos Kosmidis, et al. "Suppression of connexin 43 phosphorylation promotes astrocyte survival and vascular regeneration in proliferative retinopathy." Proceedings of the National Academy of Sciences 115, no. 26 (2018): E5934—E5943. http://dx.doi.org/10.1073/pnas.1803907115.

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Degeneration of retinal astrocytes precedes hypoxia-driven pathologic neovascularization and vascular leakage in ischemic retinopathies. However, the molecular events that underlie astrocyte loss remain unclear. Astrocytes abundantly express connexin 43 (Cx43), a transmembrane protein that forms gap junction (GJ) channels and hemichannels. Cx channels can transfer toxic signals from dying cells to healthy neighbors under pathologic conditions. Here we show that Cx43 plays a critical role in astrocyte apoptosis and the resulting preretinal neovascularization in a mouse model of oxygen-induced r

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Sueviriyapan, Natthapong, Chak Foon Tso, Erik D. Herzog, and Michael A. Henson. "Astrocytic Modulation of Neuronal Activity in the Suprachiasmatic Nucleus: Insights from Mathematical Modeling." Journal of Biological Rhythms 35, no. 3 (2020): 287–301. http://dx.doi.org/10.1177/0748730420913672.

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The suprachiasmatic nucleus (SCN) of the hypothalamus consists of a highly heterogeneous neuronal population networked together to allow precise and robust circadian timekeeping in mammals. While the critical importance of SCN neurons in regulating circadian rhythms has been extensively studied, the roles of SCN astrocytes in circadian system function are not well understood. Recent experiments have demonstrated that SCN astrocytes are circadian oscillators with the same functional clock genes as SCN neurons. Astrocytes generate rhythmic outputs that are thought to modulate neuronal activity t

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Padmashri, Ragunathan, Anand Suresh, Michael D. Boska, and Anna Dunaevsky. "Motor-Skill Learning Is Dependent on Astrocytic Activity." Neural Plasticity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/938023.

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Motor-skill learning induces changes in synaptic structure and function in the primary motor cortex through the involvement of a long-term potentiation- (LTP-) like mechanism. Although there is evidence that calcium-dependent release of gliotransmitters by astrocytes plays an important role in synaptic transmission and plasticity, the role of astrocytes in motor-skill learning is not known. To test the hypothesis that astrocytic activity is necessary for motor-skill learning, we perturbed astrocytic function using pharmacological and genetic approaches. We find that perturbation of astrocytes

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Khaspekov, L. G., and L. E. Frumkina. "Molecular mechanisms of astrocyte involvement in synaptogenesis and brain synaptic plasticity." Биохимия 88, no. 4 (2023): 614–28. http://dx.doi.org/10.31857/s0320972523040061.

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Astrocytes perform a wide range of important functions in the brain. As structural and functional components of synapses, astrocytes secrete various factors (proteins, lipids, small molecules, etc.) that bind to neuronal receptor and contribute to synaptogenesis and regulation of synaptic contacts. Astrocytic factors play a key role in the formation of neural networks undergoing short- and long-term synaptic morphological and functional rearrangements essential in the memory formation and behavior. The review summarizes the data on the molecular mechanisms mediating the involvement of astrocyt

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Ozawa, Katsuya, Masaki Nagao, Ayumu Konno, et al. "Astrocytic GPCR-Induced Ca2+ Signaling Is Not Causally Related to Local Cerebral Blood Flow Changes." International Journal of Molecular Sciences 24, no. 17 (2023): 13590. http://dx.doi.org/10.3390/ijms241713590.

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Activation of Gq-type G protein-coupled receptors (GPCRs) gives rise to large cytosolic Ca2+ elevations in astrocytes. Previous in vitro and in vivo studies have indicated that astrocytic Ca2+ elevations are closely associated with diameter changes in the nearby blood vessels, which astrocytes enwrap with their endfeet. However, the causal relationship between astrocytic Ca2+ elevations and blood vessel diameter changes has been questioned, as mice with diminished astrocytic Ca2+ signaling show normal sensory hyperemia. We addressed this controversy by imaging cortical vasculature while optoge

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Brunet, JF, I. Allaman, PJ Magistretti, and L. Pellerin. "Glycogen Metabolism as a Marker of Astrocyte Differentiation." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (2009): 51–55. http://dx.doi.org/10.1038/jcbfm.2009.207.

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Glycogen is a hallmark of mature astrocytes, but its emergence during astrocytic differentiation is unclear. Differentiation of E14 mouse neurospheres into astrocytes was induced with fetal bovine serum (FBS), Leukemia Inhibitory Factor (LIF), or Ciliary Neurotrophic Factor (CNTF). Cytochemical and enzymatic analyses showed that glycogen is present in FBS- or LIF- but not in CNTF-differentiated astrocytes. Glycogenolysis was induced in FBS- and LIF-differentiated astrocytes but glycogen resynthesis was observed only with FBS. Protein targeting to glycogen mRNA expression appeared with glial fi

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Rogers, Richard C., David H. McDougal, Sue Ritter, Emily Qualls-Creekmore, and Gerlinda E. Hermann. "Response of catecholaminergic neurons in the mouse hindbrain to glucoprivic stimuli is astrocyte dependent." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 1 (2018): R153—R164. http://dx.doi.org/10.1152/ajpregu.00368.2017.

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Hindbrain catecholaminergic (CA) neurons are required for critical autonomic, endocrine, and behavioral counterregulatory responses (CRRs) to hypoglycemia. Recent studies suggest that CRR initiation depends on hindbrain astrocyte glucose sensors (McDougal DH, Hermann GE, Rogers RC. Front Neurosci 7: 249, 2013; Rogers RC, Ritter S, Hermann GE. Am J Physiol Regul Integr Comp Physiol 310: R1102–R1108, 2016). To test the proposition that hindbrain CA responses to glucoprivation are astrocyte dependent, we utilized transgenic mice in which the calcium reporter construct (GCaMP5) was expressed selec

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Zuidema, Jonathan M., Ryan J. Gilbert, and Manoj K. Gottipati. "Biomaterial Approaches to Modulate Reactive Astroglial Response." Cells Tissues Organs 205, no. 5-6 (2018): 372–95. http://dx.doi.org/10.1159/000494667.

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Over several decades, biomaterial scientists have developed materials to spur axonal regeneration and limit secondary injury and tested these materials within preclinical animal models. Rarely, though, are astrocytes examined comprehensively when biomaterials are placed into the injury site. Astrocytes support neuronal function in the central nervous system. Following an injury, astrocytes undergo reactive gliosis and create a glial scar. The astrocytic glial scar forms a dense barrier which restricts the extension of regenerating axons through the injury site. However, there are several benef

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Mitroshina, Elena V., Mikhail I. Krivonosov, Alexander M. Pakhomov, et al. "Unravelling the Collective Calcium Dynamics of Physiologically Aged Astrocytes under a Hypoxic State In Vitro." International Journal of Molecular Sciences 24, no. 15 (2023): 12286. http://dx.doi.org/10.3390/ijms241512286.

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Astrocytes serve many functions in the brain related to maintaining nerve tissue homeostasis and regulating neuronal function, including synaptic transmission. It is assumed that astrocytes are crucial players in determining the physiological or pathological outcome of the brain aging process and the development of neurodegenerative diseases. Therefore, studies on the peculiarities of astrocyte physiology and interastrocytic signaling during aging are of utmost importance. Calcium waves are one of the main mechanisms of signal transmission between astrocytes, and in the present study we invest

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He, Tingting, Guo-Yuan Yang, and Zhijun Zhang. "Crosstalk of Astrocytes and Other Cells during Ischemic Stroke." Life 12, no. 6 (2022): 910. http://dx.doi.org/10.3390/life12060910.

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Stroke is a leading cause of death and long-term disability worldwide. Astrocytes structurally compose tripartite synapses, blood–brain barrier, and the neurovascular unit and perform multiple functions through cell-to-cell signaling of neurons, glial cells, and vasculature. The crosstalk of astrocytes and other cells is complicated and incompletely understood. Here we review the role of astrocytes in response to ischemic stroke, both beneficial and detrimental, from a cell–cell interaction perspective. Reactive astrocytes provide neuroprotection through antioxidation and antiexcitatory effect

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Gao, Qi, Mark Katakowski, Xiaoguang Chen, Yi Li, and Michael Chopp. "Human Marrow Stromal Cells Enhance Connexin43 Gap Junction Intercellular Communication in Cultured Astrocytes." Cell Transplantation 14, no. 2-3 (2005): 109–17. http://dx.doi.org/10.3727/000000005783983205.

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Human marrow stromal cells (hMSCs) provide functional benefit in rats subjected to stroke. Astrocytes are coupled into a cellular network via gap junction channels, predominantly composed of connexin-43 (Cx43) proteins. Astrocytes are believed to play a vital role in neuroprotection by providing energy substrates to neurons and by regulating the concentrations of K+ and neurotransmitters via gap junctions. We therefore investigated the effect of factors secreted by hMSCs on gap junction intercellular communication (GJIC), expression of Cx43, and phosphorylation of Cx43 in an astrocyte cell cul

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Wang, Cong, and Longxuan Li. "The critical role of KLF4 in regulating the activation of A1/A2 reactive astrocytes following ischemic stroke." Journal of Neuroinflammation 20, no. 1 (2023). http://dx.doi.org/10.1186/s12974-023-02742-9.

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Abstract Background We have previously demonstrated that the expression of kruppel-like transcription factor-4 (KLF-4) is upregulated in astrocytes following acute ischemic stroke (AIS) and found that KLF4 confers vascular protection against cerebral ischemic injury. However, the functional role of KLF4 in astrocyte after AIS is far from clear. Methods The intrinsic relationship between KLF4 and A1/A2 reactive astrocytes and the impact of astrocytic KLF4 on the activation of A1/A2 subtype astrocytes were evaluated in middle cerebral artery occlusion (MCAO) mice and oxygen–glucose deprivation a

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Sun, Xiangyi, Sili Pan, Dandan Li та ін. "Cell adhesion molecule protocadherin-γC5 ameliorates Aβ plaque pathogenesis by modulating astrocyte function in Alzheimer’s disease". Journal of Neuroscience, 22 січня 2025, e0967242025. https://doi.org/10.1523/jneurosci.0967-24.2025.

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Accumulation of astrocytes around β-amyloid (Aβ) plaques is one of the earliest neuropathological changes in Alzheimer’s disease (AD), but the underlying mechanisms and significance remain unclear. Cell adhesion molecule protocadherin-γC5 (Pcdh-γC5) has been reported to implicate in AD. Here we find elevated expression level of Pcdh-γC5 in the brain of 5×FAD mice and Aβ-treated astrocytes, and further reveal that Pcdh-γC5 deficiency leads to exacerbated Aβ deposition in 5×FAD mice. Deletion of Pcdh-γC5 impairs astrocyte migration, astrocytic response to Aβ signaling and Aβ phagocytosis in both

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Nonaka, Hideki, Takayuki Kondo, Mika Suga, et al. "Induced pluripotent stem cell‐based assays recapture multiple properties of human astrocytes." Journal of Cellular and Molecular Medicine 28, no. 7 (2024). http://dx.doi.org/10.1111/jcmm.18214.

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AbstractThe majority of the population of glial cells in the central nervous system consists of astrocytes, and impairment of astrocytes causes various disorders. It is useful to assess the multiple astrocytic properties in order to understand their complex roles in the pathophysiology. Although we can differentiate human astrocytes from induced pluripotent stem cells (iPSCs), it remains unknown how we can analyse and reveal the multiple properties of astrocytes in complexed human disease conditions. For this purpose, we tested astrocytic differentiation protocols from feeder‐free iPSCs based

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O'Leary, Liam Anuj, Claudia Belliveau, Maria Antonietta Davoli, et al. "Widespread Decrease of Cerebral Vimentin-Immunoreactive Astrocytes in Depressed Suicides." Frontiers in Psychiatry 12 (February 4, 2021). http://dx.doi.org/10.3389/fpsyt.2021.640963.

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Post-mortem investigations have implicated cerebral astrocytes immunoreactive (-IR) for glial fibrillary acidic protein (GFAP) in the etiopathology of depression and suicide. However, it remains unclear whether astrocytic subpopulations IR for other astrocytic markers are similarly affected. Astrocytes IR to vimentin (VIM) display different regional densities than GFAP-IR astrocytes in the healthy brain, and so may be differently altered in depression and suicide. To investigate this, we compared the densities of GFAP-IR astrocytes and VIM-IR astrocytes in post-mortem brain samples from depres

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Fritschi, Lea, Johanna Hedlund Lindmar, Florian Scheidl, and Kerstin Lenk. "Neuronal and Astrocytic Regulations in Schizophrenia: A Computational Modelling Study." Frontiers in Cellular Neuroscience 15 (August 26, 2021). http://dx.doi.org/10.3389/fncel.2021.718459.

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According to the tripartite synapse model, astrocytes have a modulatory effect on neuronal signal transmission. More recently, astrocyte malfunction has been associated with psychiatric diseases such as schizophrenia. Several hypotheses have been proposed on the pathological mechanisms of astrocytes in schizophrenia. For example, post-mortem examinations have revealed a reduced astrocytic density in patients with schizophrenia. Another hypothesis suggests that disease symptoms are linked to an abnormality of glutamate transmission, which is also regulated by astrocytes (glutamate hypothesis of

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Zhou, John, Neeraj Singh, James Galske, Jacob Hudobenko, Xiangyou Hu та Riqiang Yan. "BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides". Molecular Neurodegeneration 18, № 1 (2023). http://dx.doi.org/10.1186/s13024-023-00611-w.

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Abstract Background Abnormal accumulation of amyloid beta peptide (Aβ) in the brain induces a cascade of pathological changes in Alzheimer’s disease (AD), and inhibiting BACE1, which is required for Aβ generation, is therefore being explored for the treatment of AD by reducing Aβ accumulation. As Bace1 knockout mice exhibit increased number of reactive astrocytes and AD brains have reactive astrocytes that surround amyloid plaques, we investigated the role of BACE1 in astrocytes and determined whether BACE1 regulates astrocytic functions. Methods We conducted unbiased single cell RNA-seq (scRN

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Chen, Meifan, Laura Ingle, Erik J. Plautz, et al. "LZK-dependent stimulation of astrocyte reactivity promotes corticospinal axon sprouting." Frontiers in Cellular Neuroscience 16 (September 15, 2022). http://dx.doi.org/10.3389/fncel.2022.969261.

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Injury to the adult mammalian central nervous system induces compensatory plasticity of spared axons—referred to as collateral axon sprouting—that can facilitate neural recovery. The contribution of reactive astrocytes to axon sprouting remains elusive. Here, we sought to investigate the role of axon degeneration-reactive astrocytes in the regulation of collateral axon sprouting that occurs in the mouse spinal cord after unilateral photothrombotic stroke of the primary motor cortex. We identified astrocytic leucine zipper-bearing kinase (LZK) as a positive regulator of astrocyte reactivity to

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Schneider, Y., C. Gauer, M. Andert, et al. "Distinct forebrain regions define a dichotomous astrocytic profile in multiple system atrophy." Acta Neuropathologica Communications 12, no. 1 (2024). http://dx.doi.org/10.1186/s40478-023-01699-3.

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AbstractThe growing recognition of a dichotomous role of astrocytes in neurodegenerative processes has heightened the need for unraveling distinct astrocytic subtypes in neurological disorders. In multiple system atrophy (MSA), a rare, rapidly progressing atypical Parkinsonian disease characterized by increased astrocyte reactivity. However the specific contribution of astrocyte subtypes to neuropathology remains elusive. Hence, we first set out to profile glial fibrillary acidic protein levels in astrocytes across the human post mortem motor cortex, putamen, and substantia nigra of MSA patien

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Minge, Daniel, Cátia Domingos, Petr Unichenko, et al. "Heterogeneity and Development of Fine Astrocyte Morphology Captured by Diffraction-Limited Microscopy." Frontiers in Cellular Neuroscience 15 (June 4, 2021). http://dx.doi.org/10.3389/fncel.2021.669280.

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The fine processes of single astrocytes can contact many thousands of synapses whose function they can modulate through bi-directional signaling. The spatial arrangement of astrocytic processes and neuronal structures is relevant for such interactions and for the support of neuronal signaling by astrocytes. At the same time, the geometry of perisynaptic astrocyte processes is variable and dynamically regulated. Studying these fine astrocyte processes represents a technical challenge, because many of them cannot be fully resolved by diffraction-limited microscopy. Therefore, we have established

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Zeb, Salman, Huan Ye, Yuan Liu, et al. "Necroptotic kinases are involved in the reduction of depression-induced astrocytes and fluoxetine’s inhibitory effects on necroptotic kinases." Frontiers in Pharmacology 13 (January 4, 2023). http://dx.doi.org/10.3389/fphar.2022.1060954.

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The role of astrocytes in major depressive disorder has received great attention. Increasing evidence indicates that decreased astrocyte numbers in the hippocampus may be associated with depression, but the role of necroptosis in depression is unknown. Here, in a chronic unpredictable mild stress (CUMS) mouse model and a corticosterone (Cort)-induced human astrocyte injury model in vitro, we found that mice treated with chronic unpredictable mild stress for 3–5 weeks presented depressive-like behaviors and reduced body weight gain, accompanied by a reduction in astrocytes and a decrease in ast

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