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Special Issue "Neuron and Brain Maturation"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2021).

Special Issue Editors

Prof. Dr. Luca Bonfanti
E-Mail Website1 Website2
Guest Editor
Department of Veterinary Sciences, Neuroscience Institute Cavalieri Ottolenghi, University of Turin, 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, Paracelsus Medical University, 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 repair, maintenance, and implementation of neural circuit efficiency from birth to old age. Structural brain repair is hardly 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, and according to species and age as well. The progressive shift from plasticity to stability throughout life could define different degrees of maturation in specific brain regions. However, the criteria and mechanisms of “maturation” both at 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 new exciting perspectives in this research area.

This Special Issue will address:

- Molecular mechanisms for neuronal differentiation and maturation in different contexts (e.g., embryonic and adult neurogenesis, latent immature neurons);

- Better definition of neuronal maturational stages and of their molecular markers;

- Phylogenetic and evolutionary issues driving the adoption of different types of cellular plasticity;

- Cellular and functional aspects involved in differential maturation of brain regions;

- Neurodevelopmental aspects linked to time windows and regionalization of postnatal brain maturation;

- Glial cell contribution to brain maturation;

- Modulation of neuronal/brain maturation by experimental cues and/or lifestyle;

- Experimental paradigms/new technologies helping to better unravel the multifaceted aspects of neuronal 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

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Keywords

  • Neuronal precursors
  • Adult neurogenesis
  • Immature neurons
  • Neuronal plasticity
  • Neuronal differentiation
  • Ageing
  • Brain maturation
  • Brain homeostasis
  • Comparative neuroplasticity

Published Papers (15 papers)

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Research

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Article
Environmental Enrichment Induces Meningeal Niche Remodeling through TrkB-Mediated Signaling
Int. J. Mol. Sci. 2021, 22(19), 10657; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910657 - 01 Oct 2021
Viewed by 688
Abstract
Neural precursors (NPs) present in the hippocampus can be modulated by several neurogenic stimuli, including environmental enrichment (EE) acting through BDNF-TrkB signaling. We have recently identified NPs in meninges; however, the meningeal niche response to pro-neurogenic stimuli has never been investigated. To this [...] Read more.
Neural precursors (NPs) present in the hippocampus can be modulated by several neurogenic stimuli, including environmental enrichment (EE) acting through BDNF-TrkB signaling. We have recently identified NPs in meninges; however, the meningeal niche response to pro-neurogenic stimuli has never been investigated. To this aim, we analyzed the effects of EE exposure on NP distribution in mouse brain meninges. Following neurogenic stimuli, although we did not detect modification of the meningeal cell number and proliferation, we observed an increased number of neural precursors in the meninges. A lineage tracing experiment suggested that EE-induced β3-Tubulin+ immature neuronal cells present in the meninges originated, at least in part, from GLAST+ radial glia cells. To investigate the molecular mechanism responsible for meningeal reaction to EE exposure, we studied the BDNF-TrkB interaction. Treatment with ANA-12, a TrkB non-competitive inhibitor, abolished the EE-induced meningeal niche changes. Overall, these data showed, for the first time, that EE exposure induced meningeal niche remodeling through TrkB-mediated signaling. Fluoxetine treatment further confirmed the meningeal niche response, suggesting it may also respond to other pharmacological neurogenic stimuli. A better understanding of the neurogenic stimuli modulation for meninges may be useful to improve the effectiveness of neurodegenerative and neuropsychiatric treatments. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
The Presynaptic Scaffold Protein Bassoon in Forebrain Excitatory Neurons Mediates Hippocampal Circuit Maturation: Potential Involvement of TrkB Signalling
Int. J. Mol. Sci. 2021, 22(15), 7944; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22157944 - 26 Jul 2021
Viewed by 947
Abstract
A presynaptic active zone organizer protein Bassoon orchestrates numerous important functions at the presynaptic active zone. We previously showed that the absence of Bassoon exclusively in forebrain glutamatergic presynapses (BsnEmx1cKO) in mice leads to developmental disturbances in dentate gyrus (DG) [...] Read more.
A presynaptic active zone organizer protein Bassoon orchestrates numerous important functions at the presynaptic active zone. We previously showed that the absence of Bassoon exclusively in forebrain glutamatergic presynapses (BsnEmx1cKO) in mice leads to developmental disturbances in dentate gyrus (DG) affecting synaptic excitability, morphology, neurogenesis and related behaviour during adulthood. Here, we demonstrate that hyperexcitability of the medial perforant path-to-DG (MPP-DG) pathway in BsnEmx1cKO mice emerges during adolescence and is sustained during adulthood. We further provide evidence for a potential involvement of tropomyosin-related kinase B (TrkB), the high-affinity receptor for brain-derived neurotrophic factor (BDNF), mediated signalling. We detect elevated TrkB protein levels in the dorsal DG of adult mice (~3–5 months-old) but not in adolescent (~4–5 weeks-old) mice. Electrophysiological analysis reveals increased field-excitatory-postsynaptic-potentials (fEPSPs) in the DG of the adult, but not in adolescent BsnEmx1cKO mice. In line with an increased TrkB expression during adulthood in BsnEmx1cKO, blockade of TrkB normalizes the increased synaptic excitability in the DG during adulthood, while no such effect was observed in adolescence. Accordingly, neurogenesis, which has previously been found to be increased in adult BsnEmx1cKO mice, was unaffected at adolescent age. Our results suggest that Bassoon plays a crucial role in the TrkB-dependent postnatal maturation of the hippocampus. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
Life and Death of Immature Neurons in the Juvenile and Adult Primate Amygdala
Int. J. Mol. Sci. 2021, 22(13), 6691; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22136691 - 22 Jun 2021
Cited by 2 | Viewed by 527
Abstract
In recent years, a large population of immature neurons has been documented in the paralaminar nucleus of the primate amygdala. A substantial fraction of these immature neurons differentiate into mature neurons during postnatal development or following selective lesion of the hippocampus. Notwithstanding a [...] Read more.
In recent years, a large population of immature neurons has been documented in the paralaminar nucleus of the primate amygdala. A substantial fraction of these immature neurons differentiate into mature neurons during postnatal development or following selective lesion of the hippocampus. Notwithstanding a growing number of studies on the origin and fate of these immature neurons, fundamental questions about the life and death of these neurons remain. Here, we briefly summarize what is currently known about the immature neurons present in the primate ventral amygdala during development and in adulthood, as well as following selective hippocampal lesions. We provide evidence confirming that the distribution of immature neurons extends to the anterior portions of the entorhinal cortex and layer II of the perirhinal cortex. We also provide novel arguments derived from stereological estimates of the number of mature and immature neurons, which support the view that the migration of immature neurons from the lateral ventricle accompanies neuronal maturation in the primate amygdala at all ages. Finally, we propose and discuss the hypothesis that increased migration and maturation of neurons in the amygdala following hippocampal dysfunction may be linked to behavioral alterations associated with certain neurodevelopmental disorders. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
Absolute Proteome Analysis of Hippocampus, Cortex and Cerebellum in Aged and Young Mice Reveals Changes in Energy Metabolism
Int. J. Mol. Sci. 2021, 22(12), 6188; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126188 - 08 Jun 2021
Cited by 1 | Viewed by 873
Abstract
Aging is associated with a general decline of cognitive functions, and it is widely accepted that this decline results from changes in the expression of proteins involved in regulation of synaptic plasticity. However, several lines of evidence have accumulated that suggest that the [...] Read more.
Aging is associated with a general decline of cognitive functions, and it is widely accepted that this decline results from changes in the expression of proteins involved in regulation of synaptic plasticity. However, several lines of evidence have accumulated that suggest that the impaired function of the aged brain may be related to significant alterations in the energy metabolism. In the current study, we employed the label-free “Total protein approach” (TPA) method to focus on the similarities and differences in energy metabolism proteomes of young (1-month-old) and aged (22-month-old) murine brains. We quantified over 7000 proteins in each of the following three analyzed brain structures: the hippocampus, the cerebral cortex and the cerebellum. To the best of our knowledge, this is the most extensive quantitative proteomic description of energy metabolism pathways during the physiological aging of mice. The analysis demonstrates that aging does not significantly affect the abundance of total proteins in the studied brain structures, however, the levels of proteins constituting energy metabolism pathways differ significantly between young and aged mice. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
PSA Depletion Induces the Differentiation of Immature Neurons in the Piriform Cortex of Adult Mice
Int. J. Mol. Sci. 2021, 22(11), 5733; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115733 - 27 May 2021
Cited by 3 | Viewed by 1068
Abstract
Immature neurons are maintained in cortical regions of the adult mammalian brain. In rodents, many of these immature neurons can be identified in the piriform cortex based on their high expression of early neuronal markers, such as doublecortin (DCX) and the polysialylated form [...] Read more.
Immature neurons are maintained in cortical regions of the adult mammalian brain. In rodents, many of these immature neurons can be identified in the piriform cortex based on their high expression of early neuronal markers, such as doublecortin (DCX) and the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). This molecule plays critical roles in different neurodevelopmental events. Taking advantage of a DCX-CreERT2/Flox-EGFP reporter mice, we investigated the impact of targeted PSA enzymatic depletion in the piriform cortex on the fate of immature neurons. We report here that the removal of PSA accelerated the final development of immature neurons. This was revealed by a higher frequency of NeuN expression, an increase in the number of cells carrying an axon initial segment (AIS), and an increase in the number of dendrites and dendritic spines on the immature neurons. Taken together, our results demonstrated the crucial role of the PSA moiety in the protracted development of immature neurons residing outside of the neurogenic niches. More studies will be required to understand the intrinsic and extrinsic factors affecting PSA-NCAM expression to understand how the brain regulates the incorporation of these immature neurons to the established neuronal circuits of the adult brain. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
Neurogranin Regulates Adult-Born Olfactory Granule Cell Spine Density and Odor-Reward Associative Memory in Mice
Int. J. Mol. Sci. 2021, 22(8), 4269; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084269 - 20 Apr 2021
Cited by 1 | Viewed by 621
Abstract
Neurogranin (Ng) is a brain-specific postsynaptic protein, whose role in modulating Ca2+/calmodulin signaling in glutamatergic neurons has been linked to enhancement in synaptic plasticity and cognitive functions. Accordingly, Ng knock-out (Ng-ko) mice display hippocampal-dependent learning and memory impairments associated with a [...] Read more.
Neurogranin (Ng) is a brain-specific postsynaptic protein, whose role in modulating Ca2+/calmodulin signaling in glutamatergic neurons has been linked to enhancement in synaptic plasticity and cognitive functions. Accordingly, Ng knock-out (Ng-ko) mice display hippocampal-dependent learning and memory impairments associated with a deficit in long-term potentiation induction. In the adult olfactory bulb (OB), Ng is expressed by a large population of GABAergic granule cells (GCs) that are continuously generated during adult life, undergo high synaptic remodeling in response to the sensory context, and play a key role in odor processing. However, the possible implication of Ng in OB plasticity and function is yet to be investigated. Here, we show that Ng expression in the OB is associated with the mature state of adult-born GCs, where its active-phosphorylated form is concentrated at post-synaptic sites. Constitutive loss of Ng in Ng-ko mice resulted in defective spine density in adult-born GCs, while their survival remained unaltered. Moreover, Ng-ko mice show an impaired odor-reward associative memory coupled with reduced expression of the activity-dependent transcription factor Zif268 in olfactory GCs. Overall, our data support a role for Ng in the molecular mechanisms underlying GC plasticity and the formation of olfactory associative memory. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
Proliferative Capacity of Adult Mouse Brain
Int. J. Mol. Sci. 2021, 22(7), 3449; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073449 - 26 Mar 2021
Cited by 1 | Viewed by 706
Abstract
We studied cell proliferation in the postnatal mouse brain between the ages of 2 and 30 months and identified four compartments with different densities of proliferating cells. The first identified compartment corresponds to the postnatal pallial neurogenic (PPN) zone in the telencephalon; the [...] Read more.
We studied cell proliferation in the postnatal mouse brain between the ages of 2 and 30 months and identified four compartments with different densities of proliferating cells. The first identified compartment corresponds to the postnatal pallial neurogenic (PPN) zone in the telencephalon; the second to the subpallial postnatal neurogenic (SPPN) zone in the telencephalon; the third to the white matter bundles in the telencephalon; and the fourth to all brain parts outside of the other three compartments. We estimated that about 3.4 million new cells, including 0.8 million in the subgranular zone (SGZ) in the hippocampus, are produced in the PPN zone. About 21 million new cells, including 10 million in the subependymal zone (SEZ) in the lateral walls of the lateral ventricle and 2.7 million in the rostral migratory stream (RMS), are produced in the SPPN zone. The third and fourth compartments together produced about 31 million new cells. The analysis of cell proliferation in neurogenic zones shows that postnatal neurogenesis is the direct continuation of developmental neurogenesis in the telencephalon and that adult neurogenesis has characteristics of the late developmental process. As a developmental process, adult neurogenesis supports only compensatory regeneration, which is very inefficient. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
CaMKIIα Expressing Neurons to Report Activity-Related Endogenous Hypoxia upon Motor-Cognitive Challenge
Int. J. Mol. Sci. 2021, 22(6), 3164; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063164 - 20 Mar 2021
Cited by 1 | Viewed by 1074
Abstract
We previously introduced the brain erythropoietin (EPO) circle as a model to explain the adaptive ‘brain hardware upgrade’ and enhanced performance. In this fundamental circle, brain cells, challenged by motor-cognitive tasks, experience functional hypoxia, triggering the expression of EPO among other genes. We [...] Read more.
We previously introduced the brain erythropoietin (EPO) circle as a model to explain the adaptive ‘brain hardware upgrade’ and enhanced performance. In this fundamental circle, brain cells, challenged by motor-cognitive tasks, experience functional hypoxia, triggering the expression of EPO among other genes. We attested hypoxic cells by a transgenic reporter approach under the ubiquitous CAG promoter, with Hif-1α oxygen-dependent degradation-domain (ODD) fused to CreERT2-recombinase. To specifically focus on the functional hypoxia of excitatory pyramidal neurons, here, we generated CaMKIIα-CreERT2-ODD::R26R-tdTomato mice. Behavioral challenges, light-sheet microscopy, immunohistochemistry, single-cell mRNA-seq, and neuronal cultures under normoxia or hypoxia served to portray these mice. Upon complex running wheel performance as the motor-cognitive task, a distinct increase in functional hypoxic neurons was assessed immunohistochemically and confirmed three-dimensionally. In contrast, fear conditioning as hippocampal stimulus was likely too short-lived to provoke neuronal hypoxia. Transcriptome data of hippocampus under normoxia versus inspiratory hypoxia revealed increases in CA1 CaMKIIα-neurons with an immature signature, characterized by the expression of Dcx, Tbr1, CaMKIIα, Tle4, and Zbtb20, and consistent with accelerated differentiation. The hypoxia reporter response was reproduced in vitro upon neuronal maturation. To conclude, task-associated activity triggers neuronal functional hypoxia as a local and brain-wide reaction mediating adaptive neuroplasticity. Hypoxia-induced genes such as EPO drive neuronal differentiation, brain maturation, and improved performance. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Article
Structural and Functional Maturation of Rat Primary Motor Cortex Layer V Neurons
Int. J. Mol. Sci. 2020, 21(17), 6101; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176101 - 24 Aug 2020
Viewed by 980
Abstract
Rodent neocortical neurons undergo prominent postnatal development and maturation. The process is associated with structural and functional maturation of the axon initial segment (AIS), the site of action potential initiation. In this regard, cell size and optimal AIS length are interconnected. In sensory [...] Read more.
Rodent neocortical neurons undergo prominent postnatal development and maturation. The process is associated with structural and functional maturation of the axon initial segment (AIS), the site of action potential initiation. In this regard, cell size and optimal AIS length are interconnected. In sensory cortices, developmental onset of sensory input and consequent changes in network activity cause phasic AIS plasticity that can also control functional output. In non-sensory cortices, network input driving phasic events should be less prominent. We, therefore, explored the relationship between postnatal functional maturation and AIS maturation in principal neurons of the primary motor cortex layer V (M1LV), a non-sensory area of the rat brain. We hypothesized that a rather continuous process of AIS maturation and elongation would reflect cell growth, accompanied by progressive refinement of functional output properties. We found that, in the first two postnatal weeks, cell growth prompted substantial decline of neuronal input resistance, such that older neurons needed larger input current to reach rheobase and fire action potentials. In the same period, we observed the most prominent AIS elongation and significant maturation of functional output properties. Alternating phases of AIS plasticity did not occur, and changes in functional output properties were largely justified by AIS elongation. From the third postnatal week up to five months of age, cell growth, AIS elongation, and functional output maturation were marginal. Thus, AIS maturation in M1LV is a continuous process that attunes the functional output of pyramidal neurons and associates with early postnatal development to counterbalance increasing electrical leakage due to cell growth. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Review

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Review
Brain Plasticity in Humans and Model Systems: Advances, Challenges, and Future Directions
Int. J. Mol. Sci. 2021, 22(17), 9358; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179358 - 28 Aug 2021
Cited by 1 | Viewed by 1010
Abstract
Plasticity, and in particular, neurogenesis, is a promising target to treat and prevent a wide variety of diseases (e.g., epilepsy, stroke, dementia). There are different types of plasticity, which vary with age, brain region, and species. These observations stress the importance of defining [...] Read more.
Plasticity, and in particular, neurogenesis, is a promising target to treat and prevent a wide variety of diseases (e.g., epilepsy, stroke, dementia). There are different types of plasticity, which vary with age, brain region, and species. These observations stress the importance of defining plasticity along temporal and spatial dimensions. We review recent studies focused on brain plasticity across the lifespan and in different species. One main theme to emerge from this work is that plasticity declines with age but that we have yet to map these different forms of plasticity across species. As part of this effort, we discuss our recent progress aimed to identify corresponding ages across species, and how this information can be used to map temporal variation in plasticity from model systems to humans. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Review
Sex Steroids and the Shaping of the Peripubertal Brain: The Sexual-Dimorphic Set-Up of Adult Neurogenesis
Int. J. Mol. Sci. 2021, 22(15), 7984; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22157984 - 26 Jul 2021
Viewed by 1864
Abstract
Steroid hormones represent an amazing class of molecules that play pleiotropic roles in vertebrates. In mammals, during postnatal development, sex steroids significantly influence the organization of sexually dimorphic neural circuits underlying behaviors critical for survival, such as the reproductive one. During the last [...] Read more.
Steroid hormones represent an amazing class of molecules that play pleiotropic roles in vertebrates. In mammals, during postnatal development, sex steroids significantly influence the organization of sexually dimorphic neural circuits underlying behaviors critical for survival, such as the reproductive one. During the last decades, multiple studies have shown that many cortical and subcortical brain regions undergo sex steroid-dependent structural organization around puberty, a critical stage of life characterized by high sensitivity to external stimuli and a profound structural and functional remodeling of the organism. Here, we first give an overview of current data on how sex steroids shape the peripubertal brain by regulating neuroplasticity mechanisms. Then, we focus on adult neurogenesis, a striking form of persistent structural plasticity involved in the control of social behaviors and regulated by a fine-tuned integration of external and internal cues. We discuss recent data supporting that the sex steroid-dependent peripubertal organization of neural circuits involves a sexually dimorphic set-up of adult neurogenesis that in turn could be relevant for sex-specific reproductive behaviors. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Review
Effects of Mutations in TSC Genes on Neurodevelopment and Synaptic Transmission
Int. J. Mol. Sci. 2021, 22(14), 7273; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147273 - 06 Jul 2021
Cited by 1 | Viewed by 630
Abstract
Mutations in TSC1 or TSC2 genes are linked to alterations in neuronal function which ultimately lead to the development of a complex neurological phenotype. Here we review current research on the effects that reduction in TSC1 or TSC2 can produce on the developing [...] Read more.
Mutations in TSC1 or TSC2 genes are linked to alterations in neuronal function which ultimately lead to the development of a complex neurological phenotype. Here we review current research on the effects that reduction in TSC1 or TSC2 can produce on the developing neural network. A crucial feature of the disease pathophysiology appears to be an early deviation from typical neurodevelopment, in the form of structural abnormalities. Epileptic seizures are one of the primary early manifestation of the disease in the CNS, followed by intellectual deficits and autism spectrum disorders (ASD). Research using mouse models suggests that morphological brain alterations might arise from the interaction of different cellular types, and hyperexcitability in the early postnatal period might be transient. Moreover, the increased excitation-to-inhibition ratio might represent a transient compensatory adjustment to stabilize the developing network rather than a primary factor for the development of ASD symptoms. The inhomogeneous results suggest region-specificity as well as an evolving picture of functional alterations along development. Furthermore, ASD symptoms and epilepsy might originate from different but potentially overlapping mechanisms, which can explain recent observations obtained in patients. Potential treatment is determined not only by the type of medicament, but also by the time point of treatment. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Review
Modelling and Refining Neuronal Circuits with Guidance Cues: Involvement of Semaphorins
Int. J. Mol. Sci. 2021, 22(11), 6111; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22116111 - 06 Jun 2021
Viewed by 1040
Abstract
The establishment of neuronal circuits requires neurons to develop and maintain appropriate connections with cellular partners in and out the central nervous system. These phenomena include elaboration of dendritic arborization and formation of synaptic contacts, initially made in excess. Subsequently, refinement occurs, and [...] Read more.
The establishment of neuronal circuits requires neurons to develop and maintain appropriate connections with cellular partners in and out the central nervous system. These phenomena include elaboration of dendritic arborization and formation of synaptic contacts, initially made in excess. Subsequently, refinement occurs, and pruning takes places both at axonal and synaptic level, defining a homeostatic balance maintained throughout the lifespan. All these events require genetic regulations which happens cell-autonomously and are strongly influenced by environmental factors. This review aims to discuss the involvement of guidance cues from the Semaphorin family. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Review
Implications of Extended Inhibitory Neuron Development
Int. J. Mol. Sci. 2021, 22(10), 5113; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105113 - 12 May 2021
Cited by 2 | Viewed by 836
Abstract
A prolonged developmental timeline for GABA (γ-aminobutyric acid)-expressing inhibitory neurons (GABAergic interneurons) is an amplified trait in larger, gyrencephalic animals. In several species, the generation, migration, and maturation of interneurons take place over several months, in some cases persisting after birth. The late [...] Read more.
A prolonged developmental timeline for GABA (γ-aminobutyric acid)-expressing inhibitory neurons (GABAergic interneurons) is an amplified trait in larger, gyrencephalic animals. In several species, the generation, migration, and maturation of interneurons take place over several months, in some cases persisting after birth. The late integration of GABAergic interneurons occurs in a region-specific pattern, especially during the early postnatal period. These changes can contribute to the formation of functional connectivity and plasticity, especially in the cortical regions responsible for higher cognitive tasks. In this review, we discuss GABAergic interneuron development in the late gestational and postnatal forebrain. We propose the protracted development of interneurons at each stage (neurogenesis, neuronal migration, and network integration), as a mechanism for increased complexity and cognitive flexibility in larger, gyrencephalic brains. This developmental feature of interneurons also provides an avenue for environmental influences to shape neural circuit formation. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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Review
An Extracellular Perspective on CNS Maturation: Perineuronal Nets and the Control of Plasticity
Int. J. Mol. Sci. 2021, 22(5), 2434; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052434 - 28 Feb 2021
Cited by 12 | Viewed by 1916
Abstract
During restricted time windows of postnatal life, called critical periods, neural circuits are highly plastic and are shaped by environmental stimuli. In several mammalian brain areas, from the cerebral cortex to the hippocampus and amygdala, the closure of the critical period is dependent [...] Read more.
During restricted time windows of postnatal life, called critical periods, neural circuits are highly plastic and are shaped by environmental stimuli. In several mammalian brain areas, from the cerebral cortex to the hippocampus and amygdala, the closure of the critical period is dependent on the formation of perineuronal nets. Perineuronal nets are a condensed form of an extracellular matrix, which surrounds the soma and proximal dendrites of subsets of neurons, enwrapping synaptic terminals. Experimentally disrupting perineuronal nets in adult animals induces the reactivation of critical period plasticity, pointing to a role of the perineuronal net as a molecular brake on plasticity as the critical period closes. Interestingly, in the adult brain, the expression of perineuronal nets is remarkably dynamic, changing its plasticity-associated conditions, including memory processes. In this review, we aimed to address how perineuronal nets contribute to the maturation of brain circuits and the regulation of adult brain plasticity and memory processes in physiological and pathological conditions. Full article
(This article belongs to the Special Issue Neuron and Brain Maturation)
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