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Cells
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Glial Cells in Synaptic Plasticity
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Glial Cells in Synaptic Plasticity

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 10683

Special Issue Editors

Dr. Jean-Pierre Mothet

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Guest Editor
Laboratoire LuMIn UMR9024, École Normale Supérieure Paris-Saclay, Gif-sur-Yvette, France
Interests: gliotransmission; synaptic plasticity; NMDA receptors & co-agonists; dopamine
Prof. Dr. Vladimir Parpura

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Guest Editor
International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou 310053, China
Interests: gliotransmission; glutamate; astrocytes; glioblastoma multiforme
Special Issues, Collections and Topics in MDPI journals
Dr. Marta Navarrete Llinás

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Guest Editor
Instituto Cajal, CSIC, Madrid, Spain
Interests: gliotransmission; glutamate; astrocyte networks; nucleus accumbens; synaptic plasticity
Special Issues, Collections and Topics in MDPI journals
Dr. Giovanni Cirillo

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Guest Editor
Division of Human Anatomy-Neuronal Networks Morphology and Systems Biology Lab, Department of Mental, Physical Health and Preventive Medicine University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: maladaptive synaptic plasticity; reactive gliosis; neuroinflammation; spinal cord; non-invasive stimulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Three decades ago, emblematic studies brought glial cells out of the shadows and then transformed modern neuroscience. Nowadays, glial cells are recognized as active partners of neurons supporting an amazing array of functions in the developing and mature brain but also contributing to neurological and psychiatric diseases and injury processes. It appears clearly that glial cells contribute to almost every aspect of brain computation and seems to guide our daily life. The field is still expanding at an accelerating pace.

For this Special Issue, we welcome all types of manuscripts (Article, Review, Hypothesis, Opinion, Perspective) providing biological insights into the particular roles of glial cells in synaptic and circuits functional and structural plasticity and the implication to cognition in the healthy and diseased nervous system in any animal models including organoids. Emphasis will be given to emerging technological and methodological (theoretical and experimental) tools that offer new avenues to refine our understandings of glia (dys)functions in brain computation.

Dr. Jean-Pierre Mothet
Prof. Dr. Vladimir Parpura
Dr. Marta Navarrete Llinás
Dr. Giovanni Cirillo
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • glia heterogeneity
  • gliotransmission
  • neuron-glia communication
  • synaptic plasticity
  • cognition
  • neuronal circuits
  • synaptogenesis
  • diseases
  • glial calcium dynamics
  • glial signaling

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Related Special Issue

Published Papers (4 papers)

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Research

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22 pages, 5884 KiB  
Article
Interactions between the Astrocytic Volume-Regulated Anion Channel and Aquaporin 4 in Hyposmotic Regulation of Vasopressin Neuronal Activity in the Supraoptic Nucleus
by Yang Liu, Xiao-Ran Wang, Yun-Hao Jiang, Tong Li, Shuo Ling, Hong-Yang Wang, Jia-Wei Yu, Shu-Wei Jia, Xiao-Yu Liu, Chun-Mei Hou, Vladimir Parpura and Yu-Feng Wang
Cells 2023, 12(13), 1723; https://doi.org/10.3390/cells12131723 - 26 Jun 2023
Cited by 1 | Viewed by 1565
Abstract
We assessed interactions between the astrocytic volume-regulated anion channel (VRAC) and aquaporin 4 (AQP4) in the supraoptic nucleus (SON). Acute SON slices and cultures of hypothalamic astrocytes prepared from rats received hyposmotic challenge (HOC) with/without VRAC or AQP4 blockers. In acute slices, HOC [...] Read more.
We assessed interactions between the astrocytic volume-regulated anion channel (VRAC) and aquaporin 4 (AQP4) in the supraoptic nucleus (SON). Acute SON slices and cultures of hypothalamic astrocytes prepared from rats received hyposmotic challenge (HOC) with/without VRAC or AQP4 blockers. In acute slices, HOC caused an early decrease with a late rebound in the neuronal firing rate of vasopressin neurons, which required activity of astrocytic AQP4 and VRAC. HOC also caused a persistent decrease in the excitatory postsynaptic current frequency, supported by VRAC and AQP4 activity in early HOC; late HOC required only VRAC activity. These events were associated with the dynamics of glial fibrillary acidic protein (GFAP) filaments, the late retraction of which was mediated by VRAC activity; this activity also mediated an HOC-evoked early increase in AQP4 expression and late subside in GFAP-AQP4 colocalization. AQP4 activity supported an early HOC-evoked increase in VRAC levels and its colocalization with GFAP. In cultured astrocytes, late HOC augmented VRAC currents, the activation of which depended on AQP4 pre-HOC/HOC activity. HOC caused an early increase in VRAC expression followed by a late rebound, requiring AQP4 and VRAC, or only AQP4 activity, respectively. Astrocytic swelling in early HOC depended on AQP4 activity, and so did the early extension of GFAP filaments. VRAC and AQP4 activity supported late regulatory volume decrease, the retraction of GFAP filaments, and subside in GFAP-VRAC colocalization. Taken together, astrocytic morphological plasticity relies on the coordinated activities of VRAC and AQP4, which are mutually regulated in the astrocytic mediation of HOC-evoked modulation of vasopressin neuronal activity. Full article
(This article belongs to the Special Issue Glial Cells in Synaptic Plasticity)
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12 pages, 1848 KiB  
Article
Glutamate–Transporter Unbinding in Probabilistic Synaptic Environment Facilitates Activation of Distant NMDA Receptors
by Leonid P. Savtchenko and Dmitri A. Rusakov
Cells 2023, 12(12), 1610; https://doi.org/10.3390/cells12121610 - 12 Jun 2023
Cited by 1 | Viewed by 1442
Abstract
Once outside the synaptic cleft, the excitatory neurotransmitter glutamate is rapidly bound by its high-affinity transporters, which are expressed in abundance on the surface of perisynaptic astroglia. While this binding and the subsequent uptake of glutamate constrain excitatory transmission mainly within individual synapses, [...] Read more.
Once outside the synaptic cleft, the excitatory neurotransmitter glutamate is rapidly bound by its high-affinity transporters, which are expressed in abundance on the surface of perisynaptic astroglia. While this binding and the subsequent uptake of glutamate constrain excitatory transmission mainly within individual synapses, there is growing evidence for the physiologically important extrasynaptic actions of glutamate. However, the mechanistic explanation and the scope of such actions remain obscure. Furthermore, a significant proportion of glutamate molecules initially bound by transporters could be released back into the extracellular space before being translocated into astrocytes. To understand the implications of such effects, we simulated the release, diffusion, and transporter and receptor interactions of glutamate molecules in the synaptic environment. The latter was represented via trial-by-trial stochastic generation of astroglial and neuronal elements in the brain neuropil (overlapping spheroids of varied sizes), rather than using the ‘average’ morphology, thus reflecting the probabilistic nature of neuropil architectonics. Our simulations predict significant activation of high-affinity receptors, such as receptors of the NMDA type, at distances beyond half-micron from the glutamate release site, with glutamate–transporter unbinding playing an important role. These theoretical predictions are consistent with recent glutamate imaging data, thus lending support to the concept of significant volume-transmitted actions of glutamate in the brain. Full article
(This article belongs to the Special Issue Glial Cells in Synaptic Plasticity)
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28 pages, 5418 KiB  
Article
Human PSEN1 Mutant Glia Improve Spatial Learning and Memory in Aged Mice
by Henna Jäntti, Minna Oksanen, Pinja Kettunen, Stella Manta, Lionel Mouledous, Hennariikka Koivisto, Johanna Ruuth, Kalevi Trontti, Hiramani Dhungana, Meike Keuters, Isabelle Weert, Marja Koskuvi, Iiris Hovatta, Anni-Maija Linden, Claire Rampon, Tarja Malm, Heikki Tanila, Jari Koistinaho and Taisia Rolova
Cells 2022, 11(24), 4116; https://doi.org/10.3390/cells11244116 - 18 Dec 2022
Cited by 1 | Viewed by 3376
Abstract
The PSEN1 ΔE9 mutation causes a familial form of Alzheimer’s disease (AD) by shifting the processing of amyloid precursor protein (APP) towards the generation of highly amyloidogenic Aβ42 peptide. We have previously shown that the PSEN1 ΔE9 mutation in human-induced pluripotent stem cell [...] Read more.
The PSEN1 ΔE9 mutation causes a familial form of Alzheimer’s disease (AD) by shifting the processing of amyloid precursor protein (APP) towards the generation of highly amyloidogenic Aβ42 peptide. We have previously shown that the PSEN1 ΔE9 mutation in human-induced pluripotent stem cell (iPSC)-derived astrocytes increases Aβ42 production and impairs cellular responses. Here, we injected PSEN1 ΔE9 mutant astrosphere-derived glial progenitors into newborn mice and investigated mouse behavior at the ages of 8, 12, and 16 months. While we did not find significant behavioral changes in younger mice, spatial learning and memory were paradoxically improved in 16-month-old PSEN1 ΔE9 glia-transplanted male mice as compared to age-matched isogenic control-transplanted animals. Memory improvement was associated with lower levels of soluble, but not insoluble, human Aβ42 in the mouse brain. We also found a decreased engraftment of PSEN1 ΔE9 mutant cells in the cingulate cortex and significant transcriptional changes in both human and mouse genes in the hippocampus, including the extracellular matrix-related genes. Overall, the presence of PSEN1 ΔE9 mutant glia exerted a more beneficial effect on aged mouse brain than the isogenic control human cells likely as a combination of several factors. Full article
(This article belongs to the Special Issue Glial Cells in Synaptic Plasticity)
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Review

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19 pages, 1243 KiB  
Review
Shining the Light on Astrocytic Ensembles
by Laura Delgado and Marta Navarrete
Cells 2023, 12(9), 1253; https://doi.org/10.3390/cells12091253 - 26 Apr 2023
Cited by 5 | Viewed by 3189
Abstract
While neurons have traditionally been considered the primary players in information processing, the role of astrocytes in this mechanism has largely been overlooked due to experimental constraints. In this review, we propose that astrocytic ensembles are active working groups that contribute significantly to [...] Read more.
While neurons have traditionally been considered the primary players in information processing, the role of astrocytes in this mechanism has largely been overlooked due to experimental constraints. In this review, we propose that astrocytic ensembles are active working groups that contribute significantly to animal conduct and suggest that studying the maps of these ensembles in conjunction with neurons is crucial for a more comprehensive understanding of behavior. We also discuss available methods for studying astrocytes and argue that these ensembles, complementarily with neurons, code and integrate complex behaviors, potentially specializing in concrete functions. Full article
(This article belongs to the Special Issue Glial Cells in Synaptic Plasticity)
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