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Molecular Mechanisms of Neural Circuit Development and Regeneration 2.0

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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 (30 June 2022) | Viewed by 13467

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Special Issue Editors

Prof. Dr. Lieve Moons

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Guest Editor

Neural Circuit Development and Regeneration Research Group, Department of Biology, University of Leuven, Leuven, Belgium
Interests: neurodegeneration; axonal regeneration; neuroinflammation; retina; optic nerve; mouse; teleost fish; mitochondria; intraneuronal transport and communication
Special Issues, Collections and Topics in MDPI journals

Dr. Lies De Groef

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Guest Editor

Neural Circuit Development and Regeneration Research Group, Department of Biology, University of Leuven, Leuven, Belgium
Interests: neurodegeneration; neuroinflammation; retina; optic nerve; mouse; protein aggregation; Parkinson’s disease; extracellular vesicles; intercellular transport and communication
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue follows the publication of the first edition on the “Molecular Mechanisms of Neural Circuit Development and Regeneration”, which presented 13 high-quality papers.

The human brain has one hundred billion neurons, each neuron connected to ten thousand other neurons. Understanding how these neural circuits are formed and what is needed for them to be repaired is one of the biggest challenges in modern science. Studies in different animal models have helped to unravel the principles of neural circuit formation yet have also pointed out striking differences in the regenerative capacity of the central nervous system (CNS) among species. Further insights into the gene networks, molecular players, and (sub)cellular entities responsible for neural circuit formation are still urgently needed and may propel the search for neuroprotective and reparative strategies for treating neurodevelopmental and neurodegenerative conditions.

An intriguing question with respect to neural circuit formation is how this process is being orchestrated in the developing CNS, and whether this developmental program can be used to regenerate adult neural circuits. We especially encourage submissions that address the common or differential molecular and cellular mechanisms involved in neurodevelopment and regeneration, as well as other comparative research focusing on, for example, animal model organisms with different regenerative capacities, and CNS versus peripheral nervous system repair.

The Special Issue is open to original papers, reviews, and other forms of scientific communication that increase our fundamental understanding of neural circuit development and regeneration.

Prof. Dr. Lieve Moons
Dr. Lies De Groef
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. 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

Axonal development/regeneration
Axonal branching
Neurogenesis
Stem cells
Neuroprotection
Neural circuit formation
Neural circuit recovery
Regenerative potential
Central nervous system
Peripheral nervous system
Comparative research
Molecular mechanisms
Cellular mechanisms

Published Papers (3 papers)

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Research

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15 pages, 3437 KiB

Open AccessArticle

Short-Term, Voluntary Exercise Affects Morpho-Functional Maturation of Adult-Generated Neurons in Rat Hippocampus

by Davide Lattanzi, David Savelli, Marica Pagliarini, Riccardo Cuppini and Patrizia Ambrogini

Int. J. Mol. Sci. 2022, 23(12), 6866; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126866 - 20 Jun 2022

Cited by 6 | Viewed by 1782

Abstract

Physical exercise is a well-proven neurogenic stimulus, promoting neuronal progenitor proliferation and affecting newborn cell survival. Besides, it has beneficial effects on brain health and cognition. Previously, we found that three days of physical activity in a very precocious period of adult-generated granule cell life is able to antedate the appearance of the first GABAergic synaptic contacts and increase T-type Ca²⁺ channel expression. Considering the role of GABA and Ca²⁺ in fostering neuronal maturation, in this study, we used short-term, voluntary exercise on a running wheel to investigate if it is able to induce long-term morphological and synaptic changes in newborn neurons. Using adult male rats, we found that: (i) three days of voluntary physical exercise can definitively influence the morpho-functional maturation process of newborn granule neurons when applied very early during their development; (ii) a significant percentage of new neurons show more mature morphological characteristics far from the end of exercise protocol; (iii) the long-term morphological effects result in enhanced synaptic plasticity. Present findings demonstrate that the morpho-functional changes induced by exercise on very immature adult-generated neurons are permanent, affecting the neuron maturation and integration in hippocampal circuitry. Our data contribute to underpinning the beneficial potential of physical activity on brain health, also performed for short times. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Neural Circuit Development and Regeneration 2.0)

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29 pages, 4199 KiB

Open AccessArticle

A Monoclonal Anti-HMGB1 Antibody Attenuates Neurodegeneration in an Experimental Animal Model of Glaucoma

by Henrik Tonner, Selina Hunn, Nadine Auler, Carsten Schmelter, Vanessa M. Beutgen, Harald D. von Pein, Norbert Pfeiffer and Franz H. Grus

Int. J. Mol. Sci. 2022, 23(8), 4107; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23084107 - 07 Apr 2022

Cited by 11 | Viewed by 2511

Abstract

Neuroinflammation is a crucial process for the loss of retinal ganglion cells (RGC), a major characteristic of glaucoma. High expression of high-mobility group box protein 1 (HMGB1) plays a detrimental role in inflammatory processes and is elevated in the retinas of glaucoma patients. Therefore, this study aimed to investigate the effects of the intravitreal injection of an anti-HMGB1 monoclonal antibody (anti-HMGB1 Ab) in an experimental animal model of glaucoma. Two groups of Spraque Dawley rats received episcleral vein occlusion to chronically elevate intraocular pressure (IOP): (1) the IgG group, intravitreal injection of an unspecific IgG as a control, n = 5, and (2) the HMGB1 group, intravitreal injection of an anti-HMGB1 Ab, n = 6. IOP, retinal nerve fiber layer thickness (RNFLT), and the retinal flash response were monitored longitudinally. Post-mortem examinations included immunohistochemistry, microarray, and mass spectrometric analysis. RNFLT was significantly increased in the HMGB1 group compared with the IgG group (p < 0.001). RGC density showed improved neuronal cell survival in the retina in HMGB1 compared with the IgG group (p < 0.01). Mass spectrometric proteomic analysis of retinal tissue showed an increased abundance of RNA metabolism-associated heterogeneous nuclear ribonucleoproteins (hnRNPs), such as hnRNP U, D, and H2, in animals injected with the anti-HMGB1 Ab, indicating that the application of the antibody may cause increased gene expression. Microarray analysis showed a significantly decreased expression of C-X-C motif chemokine ligand 8 (CXCL8, p < 0.05) and connective tissue growth factor (CTGF, p < 0.01) in the HMGB1 group. Thus, these data suggest that intravitreal injection of anti-HMGB1 Ab reduced HMGB1-dependent inflammatory signaling and mediated RGC neuroprotection. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Neural Circuit Development and Regeneration 2.0)

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Review

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21 pages, 1082 KiB

Open AccessReview

One Raft to Guide Them All, and in Axon Regeneration Inhibit Them

by Marc Hernaiz-Llorens, Ramón Martínez-Mármol, Cristina Roselló-Busquets and Eduardo Soriano

Int. J. Mol. Sci. 2021, 22(9), 5009; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22095009 - 08 May 2021

Cited by 3 | Viewed by 8547

Abstract

Central nervous system damage caused by traumatic injuries, iatrogenicity due to surgical interventions, stroke and neurodegenerative diseases is one of the most prevalent reasons for physical disability worldwide. During development, axons must elongate from the neuronal cell body to contact their precise target cell and establish functional connections. However, the capacity of the adult nervous system to restore its functionality after injury is limited. Given the inefficacy of the nervous system to heal and regenerate after damage, new therapies are under investigation to enhance axonal regeneration. Axon guidance cues and receptors, as well as the molecular machinery activated after nervous system damage, are organized into lipid raft microdomains, a term typically used to describe nanoscale membrane domains enriched in cholesterol and glycosphingolipids that act as signaling platforms for certain transmembrane proteins. Here, we systematically review the most recent findings that link the stability of lipid rafts and their composition with the capacity of axons to regenerate and rebuild functional neural circuits after damage. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Neural Circuit Development and Regeneration 2.0)

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