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Astrocyte–Neuron Communication in Neurological Disorders

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (10 December 2022) | Viewed by 11866

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Dr. Balazs Pal

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Department of Physiology, Faculty of Medicine, University of Debrecen, 4012 Debrecen, Hungary
Interests: synapses; neuron; neurobiology; synaptic plasticity; cellular neuroscience; patch-clamp electrophysiology; calcium imaging; neuron-glia interaction; optogenetics

Special Issue Information

Dear Colleagues，

Astrocytes are electrically non-excitable members of the central nervous system. Despite this, they can effectively contribute to regulating neuronal activity in a complex manner: by regulating excitability of single neurons; cleaving excitatory neurotransmitters from the synaptic and extrasynaptic spaces; and by regulating synaptic strength. With these functions, they can influence neuronal network activity. Via this action on network activity, astrocyte–neuron communications are involved in several physiological processes such as learning or regulation of sleep-wakefulness. Astrocytes are also involved in the pathogenesis of various neurological, neuropsychiatric diseases by alterations of their actions on neurons.

In this Special Issue, submissions on a wide range of topics are invited, including research articles, reviews or mini-reviews of in vitro, ex vivo/in vivo. Submissions of manuscripts regarding age dependence of astrocyte–neuron communication or dementias, are particularly welcomed.

Dr. Balazs Pal
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

astrocyte
aging
neuronal excitability
neuromodulation
ion channels
glutamate receptors
gliotransmitters

Published Papers (4 papers)

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Research

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13 pages, 4412 KiB

Open AccessArticle

Pharmacological Activation of Piezo1 Channels Enhances Astrocyte–Neuron Communication via NMDA Receptors in the Murine Neocortex

by Andrea Csemer, Cintia Sokvári, Baneen Maamrah, László Szabó, Kristóf Korpás, Krisztina Pocsai and Balázs Pál

Int. J. Mol. Sci. 2024, 25(7), 3994; https://doi.org/10.3390/ijms25073994 - 3 Apr 2024

Viewed by 952

Abstract

The Piezo1 mechanosensitive ion channel is abundant on several elements of the central nervous system including astrocytes. It has been already demonstrated that activation of these channels is able to elicit calcium waves on astrocytes, which contributes to the release of gliotransmitters. Astrocyte- and N-methyl-D-aspartate (NMDA) receptor-dependent slow inward currents (SICs) are hallmarks of astrocyte–neuron communication. These currents are triggered by glutamate released as gliotransmitter, which in turn activates neuronal NMDA receptors responsible for this inward current having slower kinetics than any synaptic events. In this project, we aimed to investigate whether Piezo1 activation and inhibition is able to alter spontaneous SIC activity of murine neocortical pyramidal neurons. When the Piezo1 opener Yoda1 was applied, the SIC frequency and the charge transfer by these events in a minute time was significantly increased. These changes were prevented by treating the preparations with the NMDA receptor inhibitor D-AP5. Furthermore, Yoda1 did not alter the spontaneous EPSC frequency and amplitude when SICs were absent. The Piezo1 inhibitor Dooku1 effectively reverted the actions of Yoda1 and decreased the rise time of SICs when applied alone. In conclusion, activation of Piezo1 channels is able to alter astrocyte–neuron communication. Via enhancement of SIC activity, astrocytic Piezo1 channels have the capacity to determine neuronal excitability. Full article

(This article belongs to the Special Issue Astrocyte–Neuron Communication in Neurological Disorders)

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12 pages, 615 KiB

Open AccessArticle

LPS-Activated Microglial Cell-Derived Conditioned Medium Protects HT22 Neuronal Cells against Glutamate-Induced Ferroptosis

by Mauricio Tavares Jacques, Luciano Saso and Marcelo Farina

Int. J. Mol. Sci. 2023, 24(3), 2910; https://doi.org/10.3390/ijms24032910 - 2 Feb 2023

Cited by 4 | Viewed by 2696

Abstract

Neuron-glia interactions are essential for the central nervous system’s homeostasis. Microglial cells are one of the key support cells in the brain that respond to disruptions in such homeostasis. Although their participation in neuroinflammation is well known, studies investigating their role in ferroptosis, an iron-dependent form of nonapoptotic cell death, are lacking. To address this issue, we explored whether microglial (BV-2 cells) activation products can intensify, mitigate or block oxidative and/or ferroptotic damage in neuronal cells (HT22 cell line). Cultured BV-2 microglial cells were stimulated with 5–100 ng/mL lipopolysaccharide (LPS) for 24 h and, after confirmation of microglial activation, their culture medium (conditioned media; CM) was transferred to neuronal cells, which was subsequently (6 h later) exposed to glutamate or tert-butyl hydroperoxide (t-BuOOH). As a major finding, HT22 cells pretreated for 6 h with CM exhibited a significant ferroptosis-resistant phenotype characterized by decreased sensitivity to glutamate (15 mM)-induced cytotoxicity. However, no significant protective effects of LPS-activated microglial cell-derived CM were observed in t-BuOOH (30 µM)-challenged cells. In summary, activated microglia-derived molecules may protect neuronal cells against ferroptosis. The phenomenon observed in this work highlights the beneficial relationship between microglia and neurons, highlighting new possibilities for the control of ferroptosis. Full article

(This article belongs to the Special Issue Astrocyte–Neuron Communication in Neurological Disorders)

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21 pages, 17412 KiB

Open AccessArticle

Cerebral Folate Metabolism in Post-Mortem Alzheimer’s Disease Tissues: A Small Cohort Study

by Naila Naz, Syeda F. Naqvi, Nadine Hohn, Kiara Whelan, Phoebe Littler, Federico Roncaroli, Andrew C. Robinson and Jaleel A. Miyan

Int. J. Mol. Sci. 2023, 24(1), 660; https://doi.org/10.3390/ijms24010660 - 30 Dec 2022

Cited by 3 | Viewed by 2247

Abstract

We investigated the cerebral folate system in post-mortem brains and matched cerebrospinal fluid (CSF) samples from subjects with definite Alzheimer’s disease (AD) (n = 21) and neuropathologically normal brains (n = 21) using immunohistochemistry, Western blot and dot blot. In AD the CSF showed a significant decrease in 10-formyl tetrahydrofolate dehydrogenase (FDH), a critical folate binding protein and enzyme in the CSF, as well as in the main folate transporter, folate receptor alpha (FRα) and folate. In tissue, we found a switch in the pathway of folate supply to the cerebral cortex in AD compared to neurologically normal brains. FRα switched from entry through FDH-positive astrocytes in normal, to entry through glial fibrillary acidic protein (GFAP)-positive astrocytes in the AD cortex. Moreover, this switch correlated with an apparent change in metabolic direction to hypermethylation of neurons in AD. Our data suggest that the reduction in FDH in CSF prohibits FRα-folate entry via FDH-positive astrocytes and promotes entry through the GFAP pathway directly to neurons for hypermethylation. This data may explain some of the cognitive decline not attributable to the loss of neurons alone and presents a target for potential treatment. Full article

(This article belongs to the Special Issue Astrocyte–Neuron Communication in Neurological Disorders)

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Review

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31 pages, 1236 KiB

Open AccessReview

Amyotrophic Lateral Sclerosis Pathoetiology and Pathophysiology: Roles of Astrocytes, Gut Microbiome, and Muscle Interactions via the Mitochondrial Melatonergic Pathway, with Disruption by Glyphosate-Based Herbicides

by George Anderson

Int. J. Mol. Sci. 2023, 24(1), 587; https://doi.org/10.3390/ijms24010587 - 29 Dec 2022

Cited by 12 | Viewed by 5329

Abstract

The pathoetiology and pathophysiology of motor neuron loss in amyotrophic lateral sclerosis (ALS) are still to be determined, with only a small percentage of ALS patients having a known genetic risk factor. The article looks to integrate wider bodies of data on the biological underpinnings of ALS, highlighting the integrative role of alterations in the mitochondrial melatonergic pathways and systemic factors regulating this pathway across a number of crucial hubs in ALS pathophysiology, namely glia, gut, and the muscle/neuromuscular junction. It is proposed that suppression of the mitochondrial melatonergic pathway underpins changes in muscle brain-derived neurotrophic factor, and its melatonergic pathway mimic, N-acetylserotonin, leading to a lack of metabolic trophic support at the neuromuscular junction. The attenuation of the melatonergic pathway in astrocytes prevents activation of toll-like receptor agonists-induced pro-inflammatory transcription factors, NF-kB, and yin yang 1, from having a built-in limitation on inflammatory induction that arises from their synchronized induction of melatonin release. Such maintained astrocyte activation, coupled with heightened microglia reactivity, is an important driver of motor neuron susceptibility in ALS. Two important systemic factors, gut dysbiosis/permeability and pineal melatonin mediate many of their beneficial effects via their capacity to upregulate the mitochondrial melatonergic pathway in central and systemic cells. The mitochondrial melatonergic pathway may be seen as a core aspect of cellular function, with its suppression increasing reactive oxygen species (ROS), leading to ROS-induced microRNAs, thereby altering the patterning of genes induced. It is proposed that the increased occupational risk of ALS in farmers, gardeners, and sportsmen and women is intimately linked to exposure, whilst being physically active, to the widely used glyphosate-based herbicides. This has numerous research and treatment implications. Full article

(This article belongs to the Special Issue Astrocyte–Neuron Communication in Neurological Disorders)

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