Neuroplasticity of Central Nervous System in Health and Disease—Series 2

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 (30 December 2023) | Viewed by 1632

Special Issue Editor


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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
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Dear Colleagues,

The need for a Second Edition of the Special Issue “Neuroplasticity of Central Nervous System in Health and Disease” demonstrates that plasticity represents a key feature of the CNS and a hot topic in the neurosciences. To date, plasticity arises from both short- and long-term adaptive synaptic changes and the “multidirectional” interactions between neural cells and their networks, extracellular matrix, and vascular system. In this context, activated glial cells, through complex mechanisms, including neuroinflammation, failure of neurovascular coupling, and metabolic/mitochondrial dysfunction, contribute to disrupting the complex neuroglial networks underlying neural homeostasis and connectivity within brain circuits. To date, this condition, called maladaptive synaptic plasticity, might represent a common primer pathogenetic mechanism for inflammatory, neurodegenerative, and psychiatric disorders. 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 an 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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Published Papers (1 paper)

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Research

25 pages, 8872 KiB  
Article
Synaptopodin Regulates Denervation-Induced Plasticity at Hippocampal Mossy Fiber Synapses
by Pia Kruse, Gudrun Brandes, Hanna Hemeling, Zhong Huang, Christoph Wrede, Jan Hegermann, Andreas Vlachos and Maximilian Lenz
Cells 2024, 13(2), 114; https://doi.org/10.3390/cells13020114 - 6 Jan 2024
Viewed by 1409
Abstract
Neurological diseases can lead to the denervation of brain regions caused by demyelination, traumatic injury or cell death. The molecular and structural mechanisms underlying lesion-induced reorganization of denervated brain regions, however, are a matter of ongoing investigation. In order to address this issue, [...] Read more.
Neurological diseases can lead to the denervation of brain regions caused by demyelination, traumatic injury or cell death. The molecular and structural mechanisms underlying lesion-induced reorganization of denervated brain regions, however, are a matter of ongoing investigation. In order to address this issue, we performed an entorhinal cortex lesion (ECL) in mouse organotypic entorhino-hippocampal tissue cultures of both sexes and studied denervation-induced plasticity of mossy fiber synapses, which connect dentate granule cells (dGCs) with CA3 pyramidal cells (CA3-PCs) and play important roles in learning and memory formation. Partial denervation caused a strengthening of excitatory neurotransmission in dGCs, CA3-PCs and their direct synaptic connections, as revealed by paired recordings (dGC-to-CA3-PC). These functional changes were accompanied by ultrastructural reorganization of mossy fiber synapses, which regularly contain the plasticity-regulating protein synaptopodin and the spine apparatus organelle. We demonstrate that the spine apparatus organelle and synaptopodin are related to ribosomes in close proximity to synaptic sites and reveal a synaptopodin-related transcriptome. Notably, synaptopodin-deficient tissue preparations that lack the spine apparatus organelle failed to express lesion-induced synaptic adjustments. Hence, synaptopodin and the spine apparatus organelle play a crucial role in regulating lesion-induced synaptic plasticity at hippocampal mossy fiber synapses. Full article
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