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Cells
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Neuroplasticity of Central Nervous System in Health and Disease
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Neuroplasticity of Central Nervous System in Health and Disease

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 (31 August 2021) | Viewed by 20980

Special Issue Editor

Dr. Giovanni Cirillo

E-Mail Website
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,

Neuroplasticity represents the key feature of the central nervous system (CNS) and includes both short- and long-term adaptive synaptic changes that, in turn, modulate the activity of brain networks underlying higher brain functions. Recent advances strongly support the role of activated glial cells in the perturbation of synaptic plasticity. This condition, called maladaptive synaptic plasticity, represents the final result of a cascade of events (neuroinflammation, failure of neurovascular coupling, changes of neurotransmitters homeostasis, failure of rescue mechanisms, metabolic/mitochondrial dysfunction) leading to disruption of the complex neuroglial networks underlying neural homeostasis and connectivity within brain circuits. In this new light, inflammatory, neurodegenerative, and also psychiatric disorders might be primarily regarded as disorders of neuroglial-based synaptic plasticity, opening new perspectives into the complex mechanisms of disease. Accordingly, the possibility to directly modulate synaptic functions and plasticity through induction of both short- and long-term neurobiological after-effects with non-invasive brain stimulation techniques is paving the way for new therapeutic strategies in treating neuropsychiatric disorders. Unraveling the complex brain structure and function at each level, from basic mechanisms to dynamic circuitry, will allow understanding of synaptic plasticity and higher brain functions and how their perturbations contribute to brain diseases.

Dr. Giovanni Cirillo
Guest Editor

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Keywords

  • synaptic plasticity
  • glial cells
  • neuroglial homeostasis
  • maladaptive plasticity
  • neuropsychiatric disorders
  • non-invasive brain stimulation techniques

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Related Special Issue

Published Papers (3 papers)

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Research

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13 pages, 5103 KiB  
Article
Altered Spinal Homeostasis and Maladaptive Plasticity in GFAP Null Mice Following Peripheral Nerve Injury
by Ciro De Luca, Assunta Virtuoso, Sohaib Ali Korai, Raffaella Cirillo, Francesca Gargano, Michele Papa and Giovanni Cirillo
Cells 2022, 11(7), 1224; https://doi.org/10.3390/cells11071224 - 5 Apr 2022
Cited by 9 | Viewed by 2943
Abstract
The maladaptive response of the central nervous system (CNS) following nerve injury is primarily linked to the activation of glial cells (reactive gliosis) that produce an inflammatory reaction and a wide cellular morpho-structural and functional/metabolic remodeling. Glial acidic fibrillary protein (GFAP), a major [...] Read more.
The maladaptive response of the central nervous system (CNS) following nerve injury is primarily linked to the activation of glial cells (reactive gliosis) that produce an inflammatory reaction and a wide cellular morpho-structural and functional/metabolic remodeling. Glial acidic fibrillary protein (GFAP), a major protein constituent of astrocyte intermediate filaments (IFs), is the hallmark of the reactive astrocytes, has pleiotropic functions and is significantly upregulated in the spinal cord after nerve injury. Here, we investigated the specific role of GFAP in glial reaction and maladaptive spinal cord plasticity following sciatic nerve spared nerve injury (SNI) in GFAP KO and wild-type (WT) animals. We evaluated the neuropathic behavior (thermal hyperalgesia, allodynia) and the expression of glial (vimentin, Iba1) and glutamate/GABA system markers (GLAST, GLT1, EAAC1, vGLUT, vGAT, GAD) in lumbar spinal cord sections of KO/WT animals. SNI induced neuropathic behavior in both GFAP KO and WT mice, paralleled by intense microglial reaction (Iba1 expression more pronounced in KO mice), reactive astrocytosis (vimentin increase) and expression remodeling of glial/neuronal glutamate/GABA transporters. In conclusion, it is conceivable that the lack of GFAP could be detrimental to the CNS as it lacks a critical sensor for neuroinflammation and morpho-functional–metabolic rewiring after nerve injury. Understanding the maladaptive morpho-functional changes of glial cells could represent the first step for a new glial-based targeted approach for mechanisms of disease in the CNS. Full article
(This article belongs to the Special Issue Neuroplasticity of Central Nervous System in Health and Disease)
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12 pages, 3084 KiB  
Article
Scavenging Tumor Necrosis Factor α Does Not Affect Inhibition of Dentate Granule Cells Following In Vitro Entorhinal Cortex Lesion
by Dimitrios Kleidonas and Andreas Vlachos
Cells 2021, 10(11), 3232; https://doi.org/10.3390/cells10113232 - 19 Nov 2021
Cited by 2 | Viewed by 2995
Abstract
Neurons that lose part of their afferent input remodel their synaptic connections. While cellular and molecular mechanisms of denervation-induced changes in excitatory neurotransmission have been identified, little is known about the signaling pathways that control inhibition in denervated networks. In this study, we [...] Read more.
Neurons that lose part of their afferent input remodel their synaptic connections. While cellular and molecular mechanisms of denervation-induced changes in excitatory neurotransmission have been identified, little is known about the signaling pathways that control inhibition in denervated networks. In this study, we used mouse entorhino-hippocampal tissue cultures of both sexes to study the role of the pro-inflammatory cytokine tumor necrosis factor α (TNFα) in denervation-induced plasticity of inhibitory neurotransmission. In line with our previous findings in vitro, an entorhinal cortex lesion triggered a compensatory increase in the excitatory synaptic strength of partially denervated dentate granule cells. Inhibitory synaptic strength was not changed 3 days after the lesion. These functional changes were accompanied by a recruitment of microglia in the denervated hippocampus, and experiments in tissue cultures prepared from TNF-reporter mice [C57BL/6-Tg(TNFa-eGFP)] showed increased TNFα expression in the denervated zone. However, inhibitory neurotransmission was not affected by scavenging TNFα with a soluble TNF receptor. In turn, a decrease in inhibition, i.e., decreased frequencies of miniature inhibitory postsynaptic currents, was observed in denervated dentate granule cells of microglia-depleted tissue cultures. We conclude from these results that activated microglia maintain the inhibition of denervated dentate granule cells and that TNFα is not required for the maintenance of inhibition after denervation. Full article
(This article belongs to the Special Issue Neuroplasticity of Central Nervous System in Health and Disease)
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Review

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34 pages, 785 KiB  
Review
Neurotherapeutics for Attention Deficit/Hyperactivity Disorder (ADHD): A Review
by Katya Rubia, Samuel Westwood, Pascal-M. Aggensteiner and Daniel Brandeis
Cells 2021, 10(8), 2156; https://doi.org/10.3390/cells10082156 - 21 Aug 2021
Cited by 42 | Viewed by 14221
Abstract
This review focuses on the evidence for neurotherapeutics for attention deficit/hyperactivity disorder (ADHD). EEG-neurofeedback has been tested for about 45 years, with the latest meta-analyses of randomised controlled trials (RCT) showing small/medium effects compared to non-active controls only. Three small studies piloted neurofeedback [...] Read more.
This review focuses on the evidence for neurotherapeutics for attention deficit/hyperactivity disorder (ADHD). EEG-neurofeedback has been tested for about 45 years, with the latest meta-analyses of randomised controlled trials (RCT) showing small/medium effects compared to non-active controls only. Three small studies piloted neurofeedback of frontal activations in ADHD using functional magnetic resonance imaging or near-infrared spectroscopy, finding no superior effects over control conditions. Brain stimulation has been applied to ADHD using mostly repetitive transcranial magnetic and direct current stimulation (rTMS/tDCS). rTMS has shown mostly negative findings on improving cognition or symptoms. Meta-analyses of tDCS studies targeting mostly the dorsolateral prefrontal cortex show small effects on cognitive improvements with only two out of three studies showing clinical improvements. Trigeminal nerve stimulation has been shown to improve ADHD symptoms with medium effect in one RCT. Modern neurotherapeutics are attractive due to their relative safety and potential neuroplastic effects. However, they need to be thoroughly tested for clinical and cognitive efficacy across settings and beyond core symptoms and for their potential for individualised treatment. Full article
(This article belongs to the Special Issue Neuroplasticity of Central Nervous System in Health and Disease)
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