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Neural Signaling, Neuromodulation and Plasticity
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Neural Signaling, Neuromodulation and Plasticity

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 (31 December 2021) | Viewed by 4917

Special Issue Editor

Prof. Dr. Metin Akay

E-Mail Website
Guest Editor
Biomedical Engineering Department, University of Houston, 3517 Cullen Blvd, Houston, TX 77204, USA
Interests: neural signaling; neuromodulation and plasticity; optogenetics; neuroscience; groundbreaking discoveries
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurons are capable of sensing and responding to changes in their microenvironments via several receptors and channels. These highly diverse receptors and channels represent the dynamics of neuronal development and plasticity, which involve multiple highly complex, interactive, and dynamic signaling pathways.

To further understand the underlying complex molecular and cellular mechanisms behind neural signaling pathways and plasticity, in this Special Issue we aim to focus on:

1) The computational modeling of neural signaling and pathways;

2) Spatial synaptic modeling;

3) The interaction between spatial and temporal mapping and synaptic plasticity;

4) The influence of individual signaling pathways on the regulation of neural stem cells.

Prof. Dr. Metin Akay
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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neural development
  • gene regularity pathways
  • neural plasticity
  • neural cell signaling
  • modelling
  • neuromodulation

Published Papers (2 papers)

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Research

16 pages, 5327 KiB  
Article
Induction of PLXNA4 Gene during Neural Differentiation in Human Umbilical-Cord-Derived Mesenchymal Stem Cells by Low-Intensity Sub-Sonic Vibration
by Hyunjin Cho, Hee-Jung Park and Young-Kwon Seo
Int. J. Mol. Sci. 2022, 23(3), 1522; https://doi.org/10.3390/ijms23031522 - 28 Jan 2022
Cited by 2 | Viewed by 1834
Abstract
Human umbilical-cord-derived mesenchymal stem cells (hUC-MSC) are a type of mesenchymal stem cells and are more primitive than other MSCs. In this study, we identify novel genes and signal-activating proteins involved in the neural differentiation of hUC-MSCs induced by Low-Intensity Sub-Sonic Vibration (LISSV). [...] Read more.
Human umbilical-cord-derived mesenchymal stem cells (hUC-MSC) are a type of mesenchymal stem cells and are more primitive than other MSCs. In this study, we identify novel genes and signal-activating proteins involved in the neural differentiation of hUC-MSCs induced by Low-Intensity Sub-Sonic Vibration (LISSV). RNA sequencing was used to find genes involved in the differentiation process by LISSV. The changes in hUC-MSCs caused by LISSV were confirmed by PLXNA4 overexpression and gene knockdown through small interfering RNA experiments. The six genes were increased among genes related to neurons and the nervous system. One of them, the PLXNA4 gene, is known to play a role as a guide for axons in the development of the nervous system. When the PLXNA4 recombinant protein was added, neuron-related genes were increased. In the PLXNA4 gene knockdown experiment, the expression of neuron-related genes was not changed by LISSV exposure. The PLXNA4 gene is activated by sema family ligands. The expression of SEMA3A was increased by LISSV, and its downstream signaling molecule, FYN, was also activated. We suggest that the PLXNA4 gene plays an important role in hUC-MSC neuronal differentiation through exposure to LISSV. The differentiation process depends on SEMA3A-PLXNA4-dependent FYN activation in hUC-MSCs. Full article
(This article belongs to the Special Issue Neural Signaling, Neuromodulation and Plasticity)
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10 pages, 3526 KiB  
Communication
Astrocyte Ca2+ Waves and Subsequent Non-Synchronized Ca2+ Oscillations Coincide with Arteriole Diameter Changes in Response to Spreading Depolarization
by Réka Tóth, Attila E. Farkas, István A. Krizbai, Péter Makra, Ferenc Bari, Eszter Farkas and Ákos Menyhárt
Int. J. Mol. Sci. 2021, 22(7), 3442; https://doi.org/10.3390/ijms22073442 - 26 Mar 2021
Cited by 1 | Viewed by 2526
Abstract
Spreading depolarization (SD) is a wave of mass depolarization that causes profound perfusion changes in acute cerebrovascular diseases. Although the astrocyte response is secondary to the neuronal depolarization with SD, it remains to be explored how glial activity is altered after the passage [...] Read more.
Spreading depolarization (SD) is a wave of mass depolarization that causes profound perfusion changes in acute cerebrovascular diseases. Although the astrocyte response is secondary to the neuronal depolarization with SD, it remains to be explored how glial activity is altered after the passage of SD. Here, we describe post-SD high frequency astrocyte Ca2+ oscillations in the mouse somatosensory cortex. The intracellular Ca2+ changes of SR101 labeled astrocytes and the SD-related arteriole diameter variations were simultaneously visualized by multiphoton microscopy in anesthetized mice. Post-SD astrocyte Ca2+ oscillations were identified as Ca2+ events non-synchronized among astrocytes in the field of view. Ca2+ oscillations occurred minutes after the Ca2+ wave of SD. Furthermore, fewer astrocytes were involved in Ca2+ oscillations at a given time, compared to Ca2+ waves, engaging all astrocytes in the field of view simultaneously. Finally, our data confirm that astrocyte Ca2+ waves coincide with arteriolar constriction, while post-SD Ca2+ oscillations occur with the peak of the SD-related vasodilation. This is the first in vivo study to present the post-SD astrocyte Ca2+ oscillations. Our results provide novel insight into the spatio-temporal correlation between glial reactivity and cerebral arteriole diameter changes behind the SD wavefront. Full article
(This article belongs to the Special Issue Neural Signaling, Neuromodulation and Plasticity)
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