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Neuron and Brain Maturation 2.0
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Neuron and Brain Maturation 2.0

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 (15 April 2023) | Viewed by 21067

Special Issue Editors

Dr. Luca Bonfanti

E-Mail Website
Guest Editor
Department of Veterinary Sciences, Neuroscience Institute Cavalieri Ottolenghi, University of Turin, 10095 Turin, Italy
Interests: brain plasticity; comparative neuroplasticity; neuronal differentiation; adult neurogenesis; immature neurons; postnatal brain development
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Sebastien Couillard-Despres

E-Mail Website1 Website2
Guest Editor
Institute of Experimental Neuroregeneration, Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, 5020 Salzburg, Austria
Interests: spinal cord injury; adult neurogenesis; neuronal precursors; piriform cortex; electrophysiology; extracellular vesicles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain structural plasticity is important for the repair, maintenance, and implementation of neural circuit efficiency from birth to old age. Structural brain repair is barely attainable in most neurological diseases. Nevertheless, structural plasticity according to lifestyle has remarkable preventive potential.

Brain plasticity involves diverse mechanisms and cell populations across different brain regions as well as varying according to species and age. The progressive shift from plasticity to stability throughout life can define different degrees of maturation in specific brain regions. However, the criteria and mechanisms of “maturation” at both the cellular level (differentiation of young nerve cells in a postnatal brain) and at the circuit level (maturation of whole brain regions) still remain elusive. Furthermore, the recent detection of prenatally settled “immature” neurons resuming maturation and functional integration in various regions of the adult brain further add to the complexity and intertwinement of neuronal and brain maturation processes. The possible contribution of such latent immature neurons to the functional homeostasis and adaptation of the adult brain opens exciting new perspectives in this research area.

This Special Issue will address:

  • Molecular mechanisms for neuronal quiescence, differentiation, and maturation in different contexts (e.g., embryonic and adult neurogenesis, latent immature neurons);
  • Better identification and characterization of neuronal maturational stages and of their transcriptomic or molecular markers;
  • Phylogenetic and evolutionary choices for different types of cellular plasticity;
  • Molecular mechanisms behind the processes of neuronal dematuration, hypo-maturation, and rejuvenation;
  • Cellular and functional aspects involved in neuronal maturation within the infant and adult brain;
  • Cognitive and behavioral aspects of neuronal maturation in the infant and adult brain;
  • Temporal and regional aspects of postnatal brain maturation;
  • Glial cell contribution to neuronal and brain maturation;
  • Modulation of neuronal and brain maturation through experimental cues, lifestyle, and pathological conditions;
  • Experimental paradigms, new technologies, and new imaging strategies that help to better unravel the multifaceted aspects of neuronal and brain maturation;
  • Choice of animal models to address the issue of brain maturation.

Prof. Dr. Luca Bonfanti
Prof. Dr. Sebastien Couillard-Despres
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

  • neuronal precursors
  • adult neurogenesis
  • immature neurons
  • neuronal plasticity
  • neuronal differentiation
  • aging and neurological disorders
  • brain maturation
  • dematuration, dedifferentiation, hypomaturation, rejuvenation
  • brain homeostasis
  • comparative neuroplasticity
  • neuron–glia interactions
  • lifestyle and behavior

Published Papers (6 papers)

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Editorial

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4 pages, 626 KiB  
Editorial
Neuron and Brain Maturation 2.0
by Luca Bonfanti and Sébastien Couillard-Després
Int. J. Mol. Sci. 2023, 24(23), 17113; https://doi.org/10.3390/ijms242317113 - 4 Dec 2023
Viewed by 798
Abstract
The mammalian central nervous system (CNS) is built up during embryogenesis by neural stem cells located in the periventricular germinal layers which undergo multiple division cycles [...] Full article
(This article belongs to the Special Issue Neuron and Brain Maturation 2.0)
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Research

Jump to: Editorial, Review

15 pages, 533 KiB  
Article
Absence of Depressive and Anxious Behavior with Genetic Dysregulation in Adult C57Bl/6J Mice after Prenatal Exposure to Ionizing Radiation
by Christine Lalonde, Shayenthiran Sreetharan, Alyssa Murray, Lisa Stoa, Mary Ellen Cybulski, Allison Kennedy, Nicholas Landry, Amy Stillar, Sandhya Khurana, Sujeenthar Tharmalingam, Joanna Wilson, Neelam Khaper, Simon J. Lees, Douglas Boreham and T. C. Tai
Int. J. Mol. Sci. 2023, 24(10), 8466; https://doi.org/10.3390/ijms24108466 - 9 May 2023
Viewed by 1892
Abstract
The exposure of ionizing radiation during early gestation often leads to deleterious and even lethal effects; however, few extensive studies have been conducted on late gestational exposures. This research examined the behavior al effects of C57Bl/6J mouse offspring exposed to low dose ionizing [...] Read more.
The exposure of ionizing radiation during early gestation often leads to deleterious and even lethal effects; however, few extensive studies have been conducted on late gestational exposures. This research examined the behavior al effects of C57Bl/6J mouse offspring exposed to low dose ionizing gamma irradiation during the equivalent third trimester. Pregnant dams were randomly assigned to sham or exposed groups to either low dose or sublethal dose radiation (50, 300, or 1000 mGy) at gestational day 15. Adult offspring underwent a behavioral and genetic analysis after being raised under normal murine housing conditions. Our results indicate very little change in the behavioral tasks measuring general anxiety, social anxiety, and stress-management in animals exposed prenatally across the low dose radiation conditions. Quantitative real-time polymerase chain reactions were conducted on the cerebral cortex, hippocampus, and cerebellum of each animal; results indicate some dysregulation in markers of DNA damage, synaptic activity, reactive oxygen species (ROS) regulation, and methylation pathways in the offspring. Together, our results provide evidence in the C57Bl/6J strain, that exposure to sublethal dose radiation (<1000 mGy) during the last period of gestation leads to no observable changes in behaviour when assessed as adults, although some changes in gene expression were observed for specific brain regions. These results indicate that the level of oxidative stress occurring during late gestation for this mouse strain is not sufficient for a change in the assessed behavioral phenotype, but results in some modest dysregulation of the genetic profile of the brain. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation 2.0)
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29 pages, 17027 KiB  
Article
Consistency and Variation in Doublecortin and Ki67 Antigen Detection in the Brain Tissue of Different Mammals, including Humans
by Marco Ghibaudi, Alessia Amenta, Miriam Agosti, Marco Riva, Jean-Marie Graïc, Francesco Bifari and Luca Bonfanti
Int. J. Mol. Sci. 2023, 24(3), 2514; https://doi.org/10.3390/ijms24032514 - 28 Jan 2023
Cited by 3 | Viewed by 2950
Abstract
Recently, a population of “immature” neurons generated prenatally, retaining immaturity for long periods and finally integrating in adult circuits has been described in the cerebral cortex. Moreover, comparative studies revealed differences in occurrence/rate of different forms of neurogenic plasticity across mammals, the “immature” [...] Read more.
Recently, a population of “immature” neurons generated prenatally, retaining immaturity for long periods and finally integrating in adult circuits has been described in the cerebral cortex. Moreover, comparative studies revealed differences in occurrence/rate of different forms of neurogenic plasticity across mammals, the “immature” neurons prevailing in gyrencephalic species. To extend experimentation from laboratory mice to large-brained mammals, including humans, it is important to detect cell markers of neurogenic plasticity in brain tissues obtained from different procedures (e.g., post-mortem/intraoperative specimens vs. intracardiac perfusion). This variability overlaps with species-specific differences in antigen distribution or antibody species specificity, making it difficult for proper comparison. In this work, we detect the presence of doublecortin and Ki67 antigen, markers for neuronal immaturity and cell division, in six mammals characterized by widely different brain size. We tested seven commercial antibodies in four selected brain regions known to host immature neurons (paleocortex, neocortex) and newly born neurons (hippocampus, subventricular zone). In selected human brains, we confirmed the specificity of DCX antibody by performing co-staining with fluorescent probe for DCX mRNA. Our results indicate that, in spite of various types of fixations, most differences were due to the use of different antibodies and the existence of real interspecies variation. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation 2.0)
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Review

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15 pages, 2209 KiB  
Review
Visual Cortical Plasticity: Molecular Mechanisms as Revealed by Induction Paradigms in Rodents
by Francisco M. Ribeiro, Miguel Castelo-Branco, Joana Gonçalves and João Martins
Int. J. Mol. Sci. 2023, 24(5), 4701; https://doi.org/10.3390/ijms24054701 - 28 Feb 2023
Viewed by 2403
Abstract
Assessing the molecular mechanism of synaptic plasticity in the cortex is vital for identifying potential targets in conditions marked by defective plasticity. In plasticity research, the visual cortex represents a target model for intense investigation, partly due to the availability of different in [...] Read more.
Assessing the molecular mechanism of synaptic plasticity in the cortex is vital for identifying potential targets in conditions marked by defective plasticity. In plasticity research, the visual cortex represents a target model for intense investigation, partly due to the availability of different in vivo plasticity-induction protocols. Here, we review two major protocols: ocular-dominance (OD) and cross-modal (CM) plasticity in rodents, highlighting the molecular signaling pathways involved. Each plasticity paradigm has also revealed the contribution of different populations of inhibitory and excitatory neurons at different time points. Since defective synaptic plasticity is common to various neurodevelopmental disorders, the potentially disrupted molecular and circuit alterations are discussed. Finally, new plasticity paradigms are presented, based on recent evidence. Stimulus-selective response potentiation (SRP) is one of the paradigms addressed. These options may provide answers to unsolved neurodevelopmental questions and offer tools to repair plasticity defects. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation 2.0)
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14 pages, 341 KiB  
Review
Triggers of Guillain–Barré Syndrome: Campylobacter jejuni Predominates
by Josef Finsterer
Int. J. Mol. Sci. 2022, 23(22), 14222; https://doi.org/10.3390/ijms232214222 - 17 Nov 2022
Cited by 25 | Viewed by 6839
Abstract
Guillain–Barré syndrome (GBS) is a rare immune-mediated acute polyradiculo-neuropathy that typically develops after a previous gastrointestinal or respiratory infection. This narrative overview aims to summarise and discuss current knowledge and previous evidence regarding triggers and pathophysiology of GBS. A systematic search of the [...] Read more.
Guillain–Barré syndrome (GBS) is a rare immune-mediated acute polyradiculo-neuropathy that typically develops after a previous gastrointestinal or respiratory infection. This narrative overview aims to summarise and discuss current knowledge and previous evidence regarding triggers and pathophysiology of GBS. A systematic search of the literature was carried out using suitable search terms. The most common subtypes of GBS are acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). The most common triggers of GBS, in three quarters of cases, are previous infections. The most common infectious agents that cause GBS include Campylobacter jejuni (C. jejuni), Mycoplasma pneumoniae, and cytomegalovirus. C. jejuni is responsible for about a third of GBS cases. GBS due to C. jejuni is usually more severe than that due to other causes. Clinical presentation of GBS is highly dependent on the structure of pathogenic lipo-oligosaccharides (LOS) that trigger the innate immune system via Toll-like-receptor (TLR)-4 signalling. AIDP is due to demyelination, whereas in AMAN, structures of the axolemma are affected in the nodal or inter-nodal space. In conclusion, GBS is a neuro-immunological disorder caused by autoantibodies against components of the myelin sheath or axolemma. Molecular mimicry between surface structures of pathogens and components of myelin or the axon is one scenario that may explain the pathophysiology of GBS. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation 2.0)
15 pages, 684 KiB  
Review
Keeping Excitation–Inhibition Ratio in Balance
by Sergei Kirischuk
Int. J. Mol. Sci. 2022, 23(10), 5746; https://doi.org/10.3390/ijms23105746 - 20 May 2022
Cited by 6 | Viewed by 4934
Abstract
Unrelated genetic mutations can lead to convergent manifestations of neurological disorders with similar behavioral phenotypes. Experimental data frequently show a lack of dramatic changes in neuroanatomy, indicating that the key cause of symptoms might arise from impairment in the communication between neurons. A [...] Read more.
Unrelated genetic mutations can lead to convergent manifestations of neurological disorders with similar behavioral phenotypes. Experimental data frequently show a lack of dramatic changes in neuroanatomy, indicating that the key cause of symptoms might arise from impairment in the communication between neurons. A transient imbalance between excitatory (glutamatergic) and inhibitory (GABAergic) synaptic transmission (the E/I balance) during early development is generally considered to underlie the development of several neurological disorders in adults. However, the E/I ratio is a multidimensional variable. Synaptic contacts are highly dynamic and the actual strength of synaptic projections is determined from the balance between synaptogenesis and synaptic elimination. During development, relatively slow postsynaptic receptors are replaced by fast ones that allow for fast stimulus-locked excitation/inhibition. Using the binomial model of synaptic transmission allows for the reassessing of experimental data from different mouse models, showing that a transient E/I shift is frequently counterbalanced by additional pre- and/or postsynaptic changes. Such changes—for instance, the slowing down of postsynaptic currents by means of immature postsynaptic receptors—stabilize the average synaptic strength, but impair the timing of information flow. Compensatory processes and/or astrocytic signaling may represent possible targets for medical treatments of different disorders directed to rescue the proper information processing. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation 2.0)
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