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Biomolecules
Special Issues
Neuron–Astrocyte Interactions in Neurological Function and Disease
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Neuron–Astrocyte Interactions in Neurological Function and Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 December 2025) | Viewed by 7954

Special Issue Editors

Dr. Micaela Zonta

E-Mail Website
Guest Editor
Istituto di Neuroscienze-CNR Consiglio Nazionale delle Ricerche, Viale Colombo 3, Padova, Italy
Interests: astrocytes; neuron–glia communication; brain physiopathology; Ca2+ imaging; neurovascular coupling; Alzheimer’s disease; epilepsy
Dr. Alessandro Di Spiezio

E-Mail Website
Guest Editor
Istituto di Neuroscienze-CNR Consiglio Nazionale delle Ricerche, Viale Colombo 3, Padova, Italy
Interests: Alzheimer’s disease; brain pathophysiology; astrocytes; neurodegenerative diseases; cellular biology

Special Issue Information

Dear Colleagues,

Astrocytes play a central role in brain homeostasis and the modulation of synaptic transmission, and the reciprocal communication between neurons and astrocytes has emerged as a key process in neurophysiology. This aspect cannot be overlooked when investigating the mechanisms involved in neuropathological conditions. Indeed, while ex vivo and in vivo findings continue to provide new insights into how astrocytes integrate neurons in modulating brain circuits and, ultimately, animal behavior, several studies on neuropathological conditions have revealed alterations in astrocyte signaling pathways, often accompanied by a shift to a reactive state and significant transcriptome changes. Viewing this Special Issue as an opportunity to disseminate recent research findings to a wide audience, we welcome reviews and research articles that address this intercommunication at structural, molecular and cellular levels, with a particular focus on findings related to neurological function and dysfunction.

Dr. Micaela Zonta
Dr. Alessandro Di Spiezio
Guest Editors

Manuscript Submission Information

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Keywords

  • astrocytes
  • neuron-astrocyte communication
  • brain function
  • neurological disease

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Published Papers (4 papers)

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Research

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24 pages, 2279 KB  
Article
Dual Oxytocin Signals in Striatal Astrocytes
by Elisa Farsetti, Sarah Amato, Monica Averna, Diego Guidolin, Marco Pedrazzi, Guido Maura, Luigi Francesco Agnati, Chiara Cervetto and Manuela Marcoli
Biomolecules 2025, 15(8), 1122; https://doi.org/10.3390/biom15081122 - 4 Aug 2025
Cited by 1 | Viewed by 1580
Abstract
The ability of the neuropeptide oxytocin to affect glial cell function is receiving increasing attention. We previously reported that oxytocin at a low nanomolar concentration could inhibit both astrocytic Ca2+ signals and glutamate release. Here, we investigate the ability of oxytocin receptors [...] Read more.
The ability of the neuropeptide oxytocin to affect glial cell function is receiving increasing attention. We previously reported that oxytocin at a low nanomolar concentration could inhibit both astrocytic Ca2+ signals and glutamate release. Here, we investigate the ability of oxytocin receptors to couple both inhibitory and stimulatory pathways in astrocytes, as already reported in neurons. We assessed the effects of oxytocin at concentrations ranging from low to high in the nanomolar range on intracellular Ca2+ signals and on the glutamate release in astrocyte processes freshly prepared from the striatum of adult rats. Our main findings are as follows: oxytocin could induce dual responses in astrocyte processes, namely the inhibition and facilitation of both Ca2+ signals and glutamate release; the inhibitory and the facilitatory response appeared dependent on activation of the Gi and the Gq pathway, respectively; both inhibitory and facilitatory responses were evoked at the same nanomolar oxytocin concentrations; and the biased agonists atosiban and carbetocin could duplicate oxytocin’s inhibitory and facilitatory response, respectively. In conclusion, due to the coupling of striatal astrocytic oxytocin receptors to different transduction pathways and the dual effects on Ca2+ signals and glutamate release, oxytocin could also play a crucial role in neuron–astrocyte bi-directional communication through a subtle regulation of striatal glutamatergic synapses. Therefore, astrocytic oxytocin receptors may offer pharmacological targets to regulate glutamatergic striatal transmission, which is potentially useful in neuropsychiatric disorders and in neurodegenerative diseases. Full article
(This article belongs to the Special Issue Neuron–Astrocyte Interactions in Neurological Function and Disease)
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18 pages, 4799 KB  
Article
Deep-Learning-Based Segmentation of Cells and Analysis (DL-SCAN)
by Alok Bhattarai, Jan Meyer, Laura Petersilie, Syed I. Shah, Louis A. Neu, Christine R. Rose and Ghanim Ullah
Biomolecules 2024, 14(11), 1348; https://doi.org/10.3390/biom14111348 - 23 Oct 2024
Cited by 3 | Viewed by 4006
Abstract
With the recent surge in the development of highly selective probes, fluorescence microscopy has become one of the most widely used approaches to studying cellular properties and signaling in living cells and tissues. Traditionally, microscopy image analysis heavily relies on manufacturer-supplied software, which [...] Read more.
With the recent surge in the development of highly selective probes, fluorescence microscopy has become one of the most widely used approaches to studying cellular properties and signaling in living cells and tissues. Traditionally, microscopy image analysis heavily relies on manufacturer-supplied software, which often demands extensive training and lacks automation capabilities for handling diverse datasets. A critical challenge arises if the fluorophores employed exhibit low brightness and a low signal-to-noise ratio (SNR). Consequently, manual intervention may become a necessity, introducing variability in the analysis outcomes even for identical samples when analyzed by different users. This leads to the incorporation of blinded analysis, which ensures that the outcome is free from user bias to a certain extent but is extremely time-consuming. To overcome these issues, we developed a tool called DL-SCAN that automatically segments and analyzes fluorophore-stained regions of interest such as cell bodies in fluorescence microscopy images using deep learning. We demonstrate the program’s ability to automate cell identification and study cellular ion dynamics using synthetic image stacks with varying SNR. This is followed by its application to experimental Na+ and Ca2+ imaging data from neurons and astrocytes in mouse brain tissue slices exposed to transient chemical ischemia. The results from DL-SCAN are consistent, reproducible, and free from user bias, allowing efficient and rapid analysis of experimental data in an objective manner. The open-source nature of the tool also provides room for modification and extension to analyze other forms of microscopy images specific to the dynamics of different ions in other cell types. Full article
(This article belongs to the Special Issue Neuron–Astrocyte Interactions in Neurological Function and Disease)
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Review

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20 pages, 1143 KB  
Review
Astrocyte Ca2+ Dysregulation in Alzheimer’s Disease Mouse Models: Revisiting the Dogma of Hyperactivity
by Alessandro Di Spiezio and Micaela Zonta
Biomolecules 2026, 16(3), 404; https://doi.org/10.3390/biom16030404 - 10 Mar 2026
Viewed by 449
Abstract
Astrocytes are essential gatekeepers of brain homeostasis, and the disruption of their functions can contribute to the development of several neurological diseases. Among astrocyte signaling pathways, the intracellular second messenger Ca2+ plays a pivotal role in regulating the release of gliotransmitters, which [...] Read more.
Astrocytes are essential gatekeepers of brain homeostasis, and the disruption of their functions can contribute to the development of several neurological diseases. Among astrocyte signaling pathways, the intracellular second messenger Ca2+ plays a pivotal role in regulating the release of gliotransmitters, which actively modulate fundamental processes in the brain such as synaptic plasticity and memory function. Several studies over the years support the idea that dysregulated astrocytic Ca2+ homeostasis represents a relevant mechanism in Alzheimer’s disease pathogenesis. Early works in transgenic mice modelling Alzheimer’s disease reported increased Ca2+ activity in astroglial cells, supporting the idea of hyperactivity as a common trait of astrocytes in this pathology. However, recent studies have described astrocyte Ca2+ hypoactivity in various mouse models, revealing a more complex and heterogeneous scenario. In this review, we summarize and critically discuss the main studies addressing the direction(s) of astrocytic Ca2+ signaling dysfunction in mouse models of Alzheimer’s disease. We prioritize investigations performed in ex vivo and in vivo conditions, carefully comparing the different experimental approaches used to measure Ca2+ activity in astrocytes. By integrating results across multiple mouse models and methodological strategies, we aim to provide a more complete picture of astrocyte Ca2+ dysregulation in Alzheimer’s disease. Full article
(This article belongs to the Special Issue Neuron–Astrocyte Interactions in Neurological Function and Disease)
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38 pages, 3246 KB  
Review
Mitochondrial Ca2+ Signaling at the Tripartite Synapse: A Unifying Framework for Glutamate Homeostasis, Metabolic Coupling, and Network Vulnerability
by Mariagrazia Mancuso, Federico Mezzalira, Beatrice Vignoli and Elisa Greotti
Biomolecules 2026, 16(1), 171; https://doi.org/10.3390/biom16010171 - 20 Jan 2026
Cited by 1 | Viewed by 913
Abstract
Mitochondrial Ca2+ signaling is increasingly recognized as a key integrator of synaptic activity, metabolism, and redox balance within the tripartite synapse. At excitatory synapses, Ca2+ influx through ionotropic glutamate receptors and voltage-gated channels is sensed and transduced by strategically positioned mitochondria, [...] Read more.
Mitochondrial Ca2+ signaling is increasingly recognized as a key integrator of synaptic activity, metabolism, and redox balance within the tripartite synapse. At excitatory synapses, Ca2+ influx through ionotropic glutamate receptors and voltage-gated channels is sensed and transduced by strategically positioned mitochondria, whose Ca2+ uptake and release tune tricarboxylic acid cycle activity, adenosine triphosphate synthesis, and reactive oxygen species (ROS) generation. Through these Ca2+-dependent processes, mitochondria are proposed to help set the threshold at which glutamatergic activity supports synaptic plasticity and homeostasis or, instead, drives hyperexcitability and excitotoxic stress. Here, we synthesize how mitochondrial Ca2+ dynamics in presynaptic terminals, postsynaptic spines, and perisynaptic astrocytic processes regulate glutamate uptake, recycling, and release, and how subtle impairments in these pathways may prime synapses for failure well before overt energetic collapse. We further examine the reciprocal interplay between Ca2+-dependent metabolic adaptations and glutamate homeostasis, the crosstalk between mitochondrial Ca2+ and ROS signals, and the distinct vulnerabilities of neuronal and astrocytic mitochondria. Finally, we discuss how disruption of this Ca2+-centered mitochondria–glutamatergic axis contributes to synaptic dysfunction and circuit vulnerability in neurodegenerative diseases, with a particular focus on Alzheimer’s disease. Full article
(This article belongs to the Special Issue Neuron–Astrocyte Interactions in Neurological Function and Disease)
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