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Special Issue "Glial Ion Channels and Transporters in Health and Disease"

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 (30 April 2021).

Special Issue Editor

Prof. Laura Bianchi
E-Mail Website
Guest Editor
University of Miami Leonard M. Miller School of Medicine, Miami, United States
Interests: ion channels; transporters; glia; neuron; C. elegans; ionic homeostasis; glia/neuron interaction; neurodegeneration; sensory; touch

Special Issue Information

Dear Colleagues,

The first description of neurons and glia is most likely synchronous. Indeed, in 1824, Henri Dutrochet reported for the first time two types of “globular corpuscules” in the ganglia of two species of mollusks: large ones (neurons) and associated smaller ones (glia). However, the concept of animal electricity had been introduced a few decades earlier by Galvani and so the study of the excitable cells of the nervous system took off, leaving the study of glia to lag. However, the 1950s started to see a surge of interest in glial cells, with a slow shift of paradigm from considering these cells as mere structural support to viewing them as major players in the function of the nervous system. In particular, the first voltage and current recordings by Coombs and colleagues (1955) and by Hillds (1958) revealed that glia are also endowed with ion channels. In the last 60+ years, we have made substantial progress in our understanding of the function of membrane proteins that mediate the transfer of ions in and out of glia, especially as it relates to neuronal output. Indeed, studies in isolated glial cells, in slices and in vivo showed that glial ion channels and transporters function in two main capacities: regulation of the ionic composition and regulation of the concentration of solutes including neurotransmitter, both by reuptake and release in the extracellular space. This Special Issue will be dedicated to highlighting research on glial ion channels and transporters that impact neuronal function and development in healthy physiology and pathology, welcoming studies that use model organisms such as C. elegans and Drosophila to decipher these functions.

Prof. Laura Bianchi
Guest Editor

Manuscript Submission Information

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Keywords

  • glia
  • ion channels
  • transporters
  • ionic homeostasis
  • neuronal function

Published Papers (4 papers)

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Research

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Open AccessArticle
Potassium Channels Kv1.3 and Kir2.1 But Not Kv1.5 Contribute to BV2 Cell Line and Primary Microglial Migration
Int. J. Mol. Sci. 2021, 22(4), 2081; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042081 - 19 Feb 2021
Cited by 1 | Viewed by 636
Abstract
(1) Background: As membrane channels contribute to different cell functions, understanding the underlying mechanisms becomes extremely important. A large number of neuronal channels have been investigated, however, less studied are the channels expressed in the glia population, particularly in microglia. In the present [...] Read more.
(1) Background: As membrane channels contribute to different cell functions, understanding the underlying mechanisms becomes extremely important. A large number of neuronal channels have been investigated, however, less studied are the channels expressed in the glia population, particularly in microglia. In the present study, we focused on the function of the Kv1.3, Kv1.5 and Kir2.1 potassium channels expressed in both BV2 cells and primary microglia cultures, which may impact the cellular migration process. (2) Methods: Using an immunocytochemical approach, we were able to show the presence of the investigated channels in BV2 microglial cells, record their currents using a patch clamp and their role in cell migration using the scratch assay. The migration of the primary microglial cells in culture was assessed using cell culture inserts. (3) Results: By blocking each potassium channel, we showed that Kv1.3 and Kir2.1 but not Kv1.5 are essential for BV2 cell migration. Further, primary microglial cultures were obtained from a line of transgenic CX3CR1-eGFP mice that express fluorescent labeled microglia. The mice were subjected to a spared nerve injury model of pain and we found that microglia motility in an 8 µm insert was reduced 2 days after spared nerve injury (SNI) compared with sham conditions. Additional investigations showed a further impact on cell motility by specifically blocking Kv1.3 and Kir2.1 but not Kv1.5; (4) Conclusions: Our study highlights the importance of the Kv1.3 and Kir2.1 but not Kv1.5 potassium channels on microglia migration both in BV2 and primary cell cultures. Full article
(This article belongs to the Special Issue Glial Ion Channels and Transporters in Health and Disease)
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Open AccessArticle
Spadin Modulates Astrocytic Passive Conductance via Inhibition of TWIK-1/TREK-1 Heterodimeric Channels
Int. J. Mol. Sci. 2020, 21(24), 9639; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249639 - 17 Dec 2020
Viewed by 489
Abstract
Astrocytes, the most abundant cell type in the brain, are non-excitable cells and play critical roles in brain function. Mature astrocytes typically exhibit a linear current–voltage relationship termed passive conductance, which is believed to enable astrocytes to maintain potassium homeostasis in the brain. [...] Read more.
Astrocytes, the most abundant cell type in the brain, are non-excitable cells and play critical roles in brain function. Mature astrocytes typically exhibit a linear current–voltage relationship termed passive conductance, which is believed to enable astrocytes to maintain potassium homeostasis in the brain. We previously demonstrated that TWIK-1/TREK-1 heterodimeric channels mainly contribute to astrocytic passive conductance. However, the molecular identity of astrocytic passive conductance is still controversial and needs to be elucidated. Here, we report that spadin, an inhibitor of TREK-1, can dramatically reduce astrocytic passive conductance in brain slices. A series of gene silencing experiments demonstrated that spadin-sensitive currents are mediated by TWIK-1/TREK-1 heterodimeric channels in cultured astrocytes and hippocampal astrocytes from brain slices. Our study clearly showed that TWIK-1/TREK-1-heterodimeric channels can act as the main molecular machinery of astrocytic passive conductance, and suggested that spadin can be used as a specific inhibitor to control astrocytic passive conductance. Full article
(This article belongs to the Special Issue Glial Ion Channels and Transporters in Health and Disease)
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Review

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Open AccessReview
Anti-Kir4.1 Antibodies in Multiple Sclerosis: Specificity and Pathogenicity
Int. J. Mol. Sci. 2020, 21(24), 9632; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249632 - 17 Dec 2020
Viewed by 542
Abstract
The glial cells in the central nervous system express diverse inward rectifying potassium channels (Kir). They express multiple Kir channel subtypes that are likely to have distinct functional roles related to their differences in conductance, and sensitivity to intracellular and extracellular factors. Dysfunction [...] Read more.
The glial cells in the central nervous system express diverse inward rectifying potassium channels (Kir). They express multiple Kir channel subtypes that are likely to have distinct functional roles related to their differences in conductance, and sensitivity to intracellular and extracellular factors. Dysfunction in a major astrocyte potassium channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurological diseases. The autoimmune effects on the potassium channel have not yet been fully described in the literature. However, several research groups have reported that the potassium channels are an immune target in patients with various neurological disorders. In 2012, Srivastava et al. reported about Kir4.1, a new immune target for autoantibodies in patients with multiple sclerosis (MS). Follow-up studies have been conducted by several research groups, but no clear conclusion has been reached. Most follow-up studies, including ours, have reported that the prevalence of Kir4.1-seropositive patients with MS was lower than that in the initial study. Therefore, we extensively review studies on the method of antibody testing, seroprevalence of MS, and other neurological diseases in patients with MS. Finally, based on the role of Kir4.1 in MS, we consider whether it could be an immune target in this disease. Full article
(This article belongs to the Special Issue Glial Ion Channels and Transporters in Health and Disease)
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Open AccessReview
The Regulation of Astrocytic Glutamate Transporters in Health and Neurodegenerative Diseases
Int. J. Mol. Sci. 2020, 21(24), 9607; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249607 - 17 Dec 2020
Viewed by 791
Abstract
The astrocytic glutamate transporters excitatory amino acid transporters 1 and 2 (EAAT1 and EAAT2) play a key role in nervous system function to maintain extracellular glutamate levels at low levels. In physiology, this is essential for the rapid uptake of synaptically released glutamate, [...] Read more.
The astrocytic glutamate transporters excitatory amino acid transporters 1 and 2 (EAAT1 and EAAT2) play a key role in nervous system function to maintain extracellular glutamate levels at low levels. In physiology, this is essential for the rapid uptake of synaptically released glutamate, maintaining the temporal fidelity of synaptic transmission. However, EAAT1/2 hypo-expression or hypo-function are implicated in several disorders, including epilepsy and neurodegenerative diseases, as well as being observed naturally with aging. This not only disrupts synaptic information transmission, but in extremis leads to extracellular glutamate accumulation and excitotoxicity. A key facet of EAAT1/2 expression in astrocytes is a requirement for signals from other brain cell types in order to maintain their expression. Recent evidence has shown a prominent role for contact-dependent neuron-to-astrocyte and/or endothelial cell-to-astrocyte Notch signalling for inducing and maintaining the expression of these astrocytic glutamate transporters. The relevance of this non-cell-autonomous dependence to age- and neurodegenerative disease-associated decline in astrocytic EAAT expression is discussed, plus the implications for disease progression and putative therapeutic strategies. Full article
(This article belongs to the Special Issue Glial Ion Channels and Transporters in Health and Disease)
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