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Cells
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New Advances in Synaptic Dysfunctions and Plasticity
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New Advances in Synaptic Dysfunctions and Plasticity

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 April 2023) | Viewed by 19629

Special Issue Editor

Dr. Andrea Marcantoni

E-Mail Website
Guest Editor
Department of Drug and Science Technology and “NIS” Inter-Departmental Centre, University of Torino, Corso Raffaello 30, 10125 Torino, Italy
Interests: mechanism of neurotransmitter release; synaptic plasticity; calcium dependent mechanisms of synaptic function; neurodegerenative diseases; classical and innovative approaches for studying synaptic activity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Synapses are the key structure involved in the modulation of brain functions. They are characterized by the ability to change activity in function of the stimulus—a unique property of neurons defined with the term of synaptic plasticity. The synaptic functions in physiological and pathological conditions have been widely studied, and classical electrophysiological approaches as well as new methods have been used to define their precise properties and alterations. The latter can impact brain development or evolve during aging. Here, we aim to collect a panoramic view of the new advances related to the knowledge of synaptic dysfunctions during neurodevelopment and neurodegeneration. Innovative strategies for the treatment of synaptopathies are crucial for this Special Issue.

Prof. Dr. Andrea Marcantoni
Guest Editor

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Keywords

  • synaptic properties
  • synaptic impairments
  • neurodevelopment
  • neurodegeneration
  • synaptopathies

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Published Papers (7 papers)

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Research

Jump to: Review, Other

19 pages, 4157 KiB  
Article
Long-Term Memory Formation in Drosophila Depends on the 3′UTR of CPEB Gene orb2
by Eugene N. Kozlov, Elena V. Tokmatcheva, Anastasia M. Khrustaleva, Eugene S. Grebenshchikov, Roman V. Deev, Rudolf A. Gilmutdinov, Lyubov A. Lebedeva, Mariya Zhukova, Elena V. Savvateeva-Popova, Paul Schedl and Yulii V. Shidlovskii
Cells 2023, 12(2), 318; https://doi.org/10.3390/cells12020318 - 14 Jan 2023
Cited by 4 | Viewed by 2944
Abstract
Activation of local translation in neurites in response to stimulation is an important step in the formation of long-term memory (LTM). CPEB proteins are a family of translation factors involved in LTM formation. The Drosophila CPEB protein Orb2 plays an important role in [...] Read more.
Activation of local translation in neurites in response to stimulation is an important step in the formation of long-term memory (LTM). CPEB proteins are a family of translation factors involved in LTM formation. The Drosophila CPEB protein Orb2 plays an important role in the development and function of the nervous system. Mutations of the coding region of the orb2 gene have previously been shown to impair LTM formation. We found that a deletion of the 3’UTR of the orb2 gene similarly results in loss of LTM in Drosophila. As a result of the deletion, the content of the Orb2 protein remained the same in the neuron soma, but significantly decreased in synapses. Using RNA immunoprecipitation followed by high-throughput sequencing, we detected more than 6000 potential Orb2 mRNA targets expressed in the Drosophila brain. Importantly, deletion of the 3′UTR of orb2 mRNA also affected the localization of the Csp, Pyd, and Eya proteins, which are encoded by putative mRNA targets of Orb2. Therefore, the 3′UTR of the orb2 mRNA is important for the proper localization of Orb2 and other proteins in synapses of neurons and the brain as a whole, providing a molecular basis for LTM formation. Full article
(This article belongs to the Special Issue New Advances in Synaptic Dysfunctions and Plasticity)
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20 pages, 5803 KiB  
Article
Maternal Hyperhomocysteinemia Produces Memory Deficits Associated with Impairment of Long-Term Synaptic Plasticity in Young Rats
by Tatyana Y. Postnikova, Dmitry V. Amakhin, Alina M. Trofimova, Natalia L. Tumanova, Nadezhda M. Dubrovskaya, Daria S. Kalinina, Anna A. Kovalenko, Anastasiia D. Shcherbitskaia, Dmitry S. Vasilev and Aleksey V. Zaitsev
Cells 2023, 12(1), 58; https://doi.org/10.3390/cells12010058 - 23 Dec 2022
Cited by 10 | Viewed by 1775
Abstract
Maternal hyperhomocysteinemia (HCY) is a common pregnancy complication caused by high levels of the homocysteine in maternal and fetal blood, which leads to the alterations of the cognitive functions, including learning and memory. In the present study, we investigated the mechanisms of these [...] Read more.
Maternal hyperhomocysteinemia (HCY) is a common pregnancy complication caused by high levels of the homocysteine in maternal and fetal blood, which leads to the alterations of the cognitive functions, including learning and memory. In the present study, we investigated the mechanisms of these alterations in a rat model of maternal HCY. The behavioral tests confirmed the memory impairments in young and adult rats following the prenatal HCY exposure. Field potential recordings in hippocampal slices demonstrated that the long-term potentiation (LTP) was significantly reduced in HCY rats. The whole-cell patch-clamp recordings in hippocampal slices demonstrated that the magnitude of NMDA receptor-mediated currents did not change while their desensitization decreased in HCY rats. No significant alterations of glutamate receptor subunit expression except GluN1 were detected in the hippocampus of HCY rats using the quantitative real-time PCR and Western blot methods. The immunofluorescence microscopy revealed that the number of synaptopodin-positive spines is reduced, while the analysis of the ultrastructure of hippocampus using the electron microscopy revealed the indications of delayed hippocampal maturation in young HCY rats. Thus, the obtained results suggest that maternal HCY disturbs the maturation of hippocampus during the first month of life, which disrupts LTP formation and causes memory impairments. Full article
(This article belongs to the Special Issue New Advances in Synaptic Dysfunctions and Plasticity)
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Review

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26 pages, 4695 KiB  
Review
Updates on the Physiopathology of Group I Metabotropic Glutamate Receptors (mGluRI)-Dependent Long-Term Depression
by Dalila Mango and Ada Ledonne
Cells 2023, 12(12), 1588; https://doi.org/10.3390/cells12121588 - 8 Jun 2023
Cited by 3 | Viewed by 2766
Abstract
Group I metabotropic glutamate receptors (mGluRI), including mGluR1 and mGluR5 subtypes, modulate essential brain functions by affecting neuronal excitability, intracellular calcium dynamics, protein synthesis, dendritic spine formation, and synaptic transmission and plasticity. Nowadays, it is well appreciated that the mGluRI-dependent long-term depression (LTD) [...] Read more.
Group I metabotropic glutamate receptors (mGluRI), including mGluR1 and mGluR5 subtypes, modulate essential brain functions by affecting neuronal excitability, intracellular calcium dynamics, protein synthesis, dendritic spine formation, and synaptic transmission and plasticity. Nowadays, it is well appreciated that the mGluRI-dependent long-term depression (LTD) of glutamatergic synaptic transmission (mGluRI-LTD) is a key mechanism by which mGluRI shapes connectivity in various cerebral circuitries, directing complex brain functions and behaviors, and that it is deranged in several neurological and psychiatric illnesses, including neurodevelopmental disorders, neurodegenerative diseases, and psychopathologies. Here, we will provide an updated overview of the physiopathology of mGluRI-LTD, by describing mechanisms of induction and regulation by endogenous mGluRI interactors, as well as functional physiological implications and pathological deviations. Full article
(This article belongs to the Special Issue New Advances in Synaptic Dysfunctions and Plasticity)
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12 pages, 1301 KiB  
Review
The Role of Ryanodine Receptors in Regulating Neuronal Activity and Its Connection to the Development of Alzheimer’s Disease
by Giuseppe Chiantia, Enis Hidisoglu and Andrea Marcantoni
Cells 2023, 12(9), 1236; https://doi.org/10.3390/cells12091236 - 25 Apr 2023
Cited by 8 | Viewed by 1773
Abstract
Research into the early impacts of Alzheimer’s disease (AD) on synapse function is one of the most promising approaches to finding a treatment. In this context, we have recently demonstrated that the Abeta42 peptide, which builds up in the brain during the processing [...] Read more.
Research into the early impacts of Alzheimer’s disease (AD) on synapse function is one of the most promising approaches to finding a treatment. In this context, we have recently demonstrated that the Abeta42 peptide, which builds up in the brain during the processing of the amyloid precursor protein (APP), targets the ryanodine receptors (RyRs) of mouse hippocampal neurons and potentiates calcium (Ca2+) release from the endoplasmic reticulum (ER). The uncontrolled increase in intracellular calcium concentration ([Ca2+]i), leading to the development of Ca2+ dysregulation events and related excitable and synaptic dysfunctions, is a consolidated hallmark of AD onset and possibly other neurodegenerative diseases. Since RyRs contribute to increasing [Ca2+]i and are thought to be a promising target for AD treatment, the goal of this review is to summarize the current level of knowledge regarding the involvement of RyRs in governing neuronal function both in physiological conditions and during the onset of AD. Full article
(This article belongs to the Special Issue New Advances in Synaptic Dysfunctions and Plasticity)
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27 pages, 1545 KiB  
Review
Synaptic Plasticity Abnormalities in Fetal Alcohol Spectrum Disorders
by Balapal S. Basavarajappa and Shivakumar Subbanna
Cells 2023, 12(3), 442; https://doi.org/10.3390/cells12030442 - 29 Jan 2023
Cited by 3 | Viewed by 2900
Abstract
The brain’s ability to strengthen or weaken synaptic connections is often termed synaptic plasticity. It has been shown to function in brain remodeling following different types of brain damage (e.g., drugs of abuse, alcohol use disorders, neurodegenerative diseases, and inflammatory conditions). Although synaptic [...] Read more.
The brain’s ability to strengthen or weaken synaptic connections is often termed synaptic plasticity. It has been shown to function in brain remodeling following different types of brain damage (e.g., drugs of abuse, alcohol use disorders, neurodegenerative diseases, and inflammatory conditions). Although synaptic plasticity mechanisms have been extensively studied, how neural plasticity can influence neurobehavioral abnormalities in alcohol use disorders (AUDs) is far from being completely understood. Alcohol use during pregnancy and its harmful effects on the developing offspring are major public health, social, and economic challenges. The significant attribute of prenatal alcohol exposure on offspring is damage to the central nervous system (CNS), causing a range of synaptic structural, functional, and behavioral impairments, collectively called fetal alcohol spectrum disorder (FASD). Although the synaptic mechanisms in FASD are limited, emerging evidence suggests that FASD pathogenesis involves altering a set of molecules involved in neurotransmission, myelination, and neuroinflammation. These studies identify several immediate and long-lasting changes using many molecular approaches that are essential for synaptic plasticity and cognitive function. Therefore, they can offer potential synaptic targets for the many neurobehavioral abnormalities observed in FASD. In this review, we discuss the substantial research progress in different aspects of synaptic and molecular changes that can shed light on the mechanism of synaptic dysfunction in FASD. Increasing our understanding of the synaptic changes in FASD will significantly advance our knowledge and could provide a basis for finding novel therapeutic targets and innovative treatment strategies. Full article
(This article belongs to the Special Issue New Advances in Synaptic Dysfunctions and Plasticity)
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20 pages, 1417 KiB  
Review
Emerging Roles of Extracellular Vesicles in Alzheimer’s Disease: Focus on Synaptic Dysfunction and Vesicle–Neuron Interaction
by Martina Gabrielli, Francesca Tozzi, Claudia Verderio and Nicola Origlia
Cells 2023, 12(1), 63; https://doi.org/10.3390/cells12010063 - 23 Dec 2022
Cited by 7 | Viewed by 3314
Abstract
Alzheimer’s disease (AD) is considered by many to be a synaptic failure. Synaptic function is in fact deeply affected in the very early disease phases and recognized as the main cause of AD-related cognitive impairment. While the reciprocal involvement of amyloid beta (Aβ) [...] Read more.
Alzheimer’s disease (AD) is considered by many to be a synaptic failure. Synaptic function is in fact deeply affected in the very early disease phases and recognized as the main cause of AD-related cognitive impairment. While the reciprocal involvement of amyloid beta (Aβ) and tau peptides in these processes is under intense investigation, the crucial role of extracellular vesicles (EVs) released by different brain cells as vehicles for these molecules and as mediators of early synaptic alterations is gaining more and more ground in the field. In this review, we will summarize the current literature on the contribution of EVs derived from distinct brain cells to neuronal alterations and build a working model for EV-mediated propagation of synaptic dysfunction in early AD. A deeper understanding of EV–neuron interaction will provide useful targets for the development of novel therapeutic approaches aimed at hampering AD progression. Full article
(This article belongs to the Special Issue New Advances in Synaptic Dysfunctions and Plasticity)
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Other

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61 pages, 1814 KiB  
Systematic Review
Dysregulated Signaling at Postsynaptic Density: A Systematic Review and Translational Appraisal for the Pathophysiology, Clinics, and Antipsychotics’ Treatment of Schizophrenia
by Andrea de Bartolomeis, Licia Vellucci, Giuseppe De Simone, Benedetta Mazza, Annarita Barone and Mariateresa Ciccarelli
Cells 2023, 12(4), 574; https://doi.org/10.3390/cells12040574 - 10 Feb 2023
Cited by 6 | Viewed by 3555
Abstract
Emerging evidence from genomics, post-mortem, and preclinical studies point to a potential dysregulation of molecular signaling at postsynaptic density (PSD) in schizophrenia pathophysiology. The PSD that identifies the archetypal asymmetric synapse is a structure of approximately 300 nm in diameter, localized behind the [...] Read more.
Emerging evidence from genomics, post-mortem, and preclinical studies point to a potential dysregulation of molecular signaling at postsynaptic density (PSD) in schizophrenia pathophysiology. The PSD that identifies the archetypal asymmetric synapse is a structure of approximately 300 nm in diameter, localized behind the neuronal membrane in the glutamatergic synapse, and constituted by more than 1000 proteins, including receptors, adaptors, kinases, and scaffold proteins. Furthermore, using FASS (fluorescence-activated synaptosome sorting) techniques, glutamatergic synaptosomes were isolated at around 70 nm, where the receptors anchored to the PSD proteins can diffuse laterally along the PSD and were stabilized by scaffold proteins in nanodomains of 50–80 nm at a distance of 20–40 nm creating “nanocolumns” within the synaptic button. In this context, PSD was envisioned as a multimodal hub integrating multiple signaling-related intracellular functions. Dysfunctions of glutamate signaling have been postulated in schizophrenia, starting from the glutamate receptor’s interaction with scaffolding proteins involved in the N-methyl-D-aspartate receptor (NMDAR). Despite the emerging role of PSD proteins in behavioral disorders, there is currently no systematic review that integrates preclinical and clinical findings addressing dysregulated PSD signaling and translational implications for antipsychotic treatment in the aberrant postsynaptic function context. Here we reviewed a critical appraisal of the role of dysregulated PSD proteins signaling in the pathophysiology of schizophrenia, discussing how antipsychotics may affect PSD structures and synaptic plasticity in brain regions relevant to psychosis. Full article
(This article belongs to the Special Issue New Advances in Synaptic Dysfunctions and Plasticity)
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