Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
4.7
Journals
Biomedicines
Special Issues
News about Structure and Function of Synapses: Health and Diseases
share announcement

News about Structure and Function of Synapses: Health and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 17618

Special Issue Editor

Prof. Dr. Jacopo Meldolesi

E-Mail Website
Guest Editor
1. San Raffaele Institute, Vita-Salute San Raffaele University, 20132 Milan, Italy
2. CNR Institute of Neuroscience, Milan-Bicocca University, 20132 Milan, Italy
Interests: neurons and their interactions with astrocytes; neurotrophin receptors; multiplicity and complexity of extracellular vesicles; non-secretory exocytosis; multiple roles of Ca2; control of gene expression; specificity of neural gene expression; neurodegenerative diseases and new therapies; synaptic pathology; astrocytes, microglia and their role in brain pathology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The general strategy of this Special Issue has been focused on the structure and function of synapses which have intensely investigated over the last few years. The main expected results allude to the significant developments of synapses. Participation in the Special Issue is obtained from the best active research groups in the world. In case contributions in synaptic areas will be submitted independently to the journal, they will first be considered and, if approved, they will be submitted for classical review evaluation.

Comprehensive reviews about synapses are approved. Please submit your title and abstract to establish a general view of the present Special Issue, available before submission of the complete reviews.

Prof. Dr. Jacopo Meldolesi
Guest Editor

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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.

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Review, Other

2 pages, 158 KiB  
Editorial
News about Structure and Function of Synapses: Health and Diseases
by Jacopo Meldolesi
Biomedicines 2022, 10(10), 2596; https://doi.org/10.3390/biomedicines10102596 - 17 Oct 2022
Viewed by 761
Abstract
During the last century, synapses have been intensely investigated as the most interesting sites of neuroscience development [...] Full article
(This article belongs to the Special Issue News about Structure and Function of Synapses: Health and Diseases)

Review

Jump to: Editorial, Other

17 pages, 962 KiB  
Review
The Role of Rab Proteins in Parkinson’s Disease Synaptopathy
by Arianna Bellucci, Francesca Longhena and Maria Grazia Spillantini
Biomedicines 2022, 10(8), 1941; https://doi.org/10.3390/biomedicines10081941 - 10 Aug 2022
Cited by 14 | Viewed by 3291
Abstract
In patients affected by Parkinson’s disease (PD), the most common neurodegenerative movement disorder, the brain is characterized by the loss of dopaminergic neurons in the nigrostriatal system, leading to dyshomeostasis of the basal ganglia network activity that is linked to motility dysfunction. PD [...] Read more.
In patients affected by Parkinson’s disease (PD), the most common neurodegenerative movement disorder, the brain is characterized by the loss of dopaminergic neurons in the nigrostriatal system, leading to dyshomeostasis of the basal ganglia network activity that is linked to motility dysfunction. PD mostly arises as an age-associated sporadic disease, but several genetic forms also exist. Compelling evidence supports that synaptic damage and dysfunction characterize the very early phases of either sporadic or genetic forms of PD and that this early PD synaptopathy drives retrograde terminal-to-cell body degeneration, culminating in neuronal loss. The Ras-associated binding protein (Rab) family of small GTPases, which is involved in the maintenance of neuronal vesicular trafficking, synaptic architecture and function in the central nervous system, has recently emerged among the major players in PD synaptopathy. In this manuscript, we provide an overview of the main findings supporting the involvement of Rabs in either sporadic or genetic PD pathophysiology, and we highlight how Rab alterations participate in the onset of early synaptic damage and dysfunction. Full article
(This article belongs to the Special Issue News about Structure and Function of Synapses: Health and Diseases)
►▼ Show Figures

Figure 1

13 pages, 626 KiB  
Review
Post-Synapses in the Brain: Role of Dendritic and Spine Structures
by Jacopo Meldolesi
Biomedicines 2022, 10(8), 1859; https://doi.org/10.3390/biomedicines10081859 - 2 Aug 2022
Cited by 6 | Viewed by 2431
Abstract
Brain synapses are neuronal structures of the greatest interest. For a long time, however, the knowledge about them was variable, and interest was mostly focused on their pre-synaptic portions, especially neurotransmitter release from axon terminals. In the present review interest is focused on [...] Read more.
Brain synapses are neuronal structures of the greatest interest. For a long time, however, the knowledge about them was variable, and interest was mostly focused on their pre-synaptic portions, especially neurotransmitter release from axon terminals. In the present review interest is focused on post-synapses, the structures receiving and converting pre-synaptic messages. Upon further modulation, such messages are transferred to dendritic fibers. Dendrites are profoundly different from axons; they are shorter and of variable thickness. Their post-synapses are of two types. Those called flat/intended/aspines, integrated into dendritic fibers, are very frequent in inhibitory neurons. The spines, small and stemming protrusions, connected to dendritic fibers by their necks, are present in almost all excitatory neurons. Several structures and functions including the post-synaptic densities and associated proteins, the nanoscale mechanisms of compartmentalization, the cytoskeletons of actin and microtubules, are analogous in the two post-synaptic forms. However other properties, such as plasticity and its functions of learning and memory, are largely distinct. Several properties of spines, including emersion from dendritic fibers, growth, change in shape and decreases in size up to disappearance, are specific. Spinal heads correspond to largely independent signaling compartments. They are motile, their local signaling is fast, however transport through their thin necks is slow. When single spines are activated separately, their dendritic effects are often lacking; when multiple spines are activated concomitantly, their effects take place. Defects of post-synaptic responses, especially those of spines, take place in various brain diseases. Here alterations affecting symptoms and future therapy are shown to occur in neurodegenerative diseases and autism spectrum disorders. Full article
(This article belongs to the Special Issue News about Structure and Function of Synapses: Health and Diseases)
►▼ Show Figures

Figure 1

16 pages, 3875 KiB  
Review
Synaptic Disruption by Soluble Oligomers in Patients with Alzheimer’s and Parkinson’s Disease
by Berenice A. Gutierrez and Agenor Limon
Biomedicines 2022, 10(7), 1743; https://doi.org/10.3390/biomedicines10071743 - 19 Jul 2022
Cited by 6 | Viewed by 2768
Abstract
Neurodegenerative diseases are the result of progressive dysfunction of the neuronal activity and subsequent neuronal death. Currently, the most prevalent neurodegenerative diseases are by far Alzheimer’s (AD) and Parkinson’s (PD) disease, affecting millions of people worldwide. Although amyloid plaques and neurofibrillary tangles are [...] Read more.
Neurodegenerative diseases are the result of progressive dysfunction of the neuronal activity and subsequent neuronal death. Currently, the most prevalent neurodegenerative diseases are by far Alzheimer’s (AD) and Parkinson’s (PD) disease, affecting millions of people worldwide. Although amyloid plaques and neurofibrillary tangles are the neuropathological hallmarks for AD and Lewy bodies (LB) are the hallmark for PD, current evidence strongly suggests that oligomers seeding the neuropathological hallmarks are more toxic and disease-relevant in both pathologies. The presence of small soluble oligomers is the common bond between AD and PD: amyloid β oligomers (AβOs) and Tau oligomers (TauOs) in AD and α-synuclein oligomers (αSynOs) in PD. Such oligomers appear to be particularly increased during the early pathological stages, targeting synapses at vulnerable brain regions leading to synaptic plasticity disruption, synapse loss, inflammation, excitation to inhibition imbalance and cognitive impairment. Absence of TauOs at synapses in individuals with strong AD disease pathology but preserved cognition suggests that mechanisms of resilience may be dependent on the interactions between soluble oligomers and their synaptic targets. In this review, we will discuss the current knowledge about the interactions between soluble oligomers and synaptic dysfunction in patients diagnosed with AD and PD, how it affects excitatory and inhibitory synaptic transmission, and the potential mechanisms of synaptic resilience in humans. Full article
(This article belongs to the Special Issue News about Structure and Function of Synapses: Health and Diseases)
►▼ Show Figures

Figure 1

20 pages, 1836 KiB  
Review
Mechanisms of Synaptic Vesicle Exo- and Endocytosis
by Sumiko Mochida
Biomedicines 2022, 10(7), 1593; https://doi.org/10.3390/biomedicines10071593 - 4 Jul 2022
Cited by 10 | Viewed by 3957
Abstract
Within 1 millisecond of action potential arrival at presynaptic terminals voltage–gated Ca2+ channels open. The Ca2+ channels are linked to synaptic vesicles which are tethered by active zone proteins. Ca2+ entrance into the active zone triggers: (1) the fusion of [...] Read more.
Within 1 millisecond of action potential arrival at presynaptic terminals voltage–gated Ca2+ channels open. The Ca2+ channels are linked to synaptic vesicles which are tethered by active zone proteins. Ca2+ entrance into the active zone triggers: (1) the fusion of the vesicle and exocytosis, (2) the replenishment of the active zone with vesicles for incoming exocytosis, and (3) various types of endocytosis for vesicle reuse, dependent on the pattern of firing. These time-dependent vesicle dynamics are controlled by presynaptic Ca2+ sensor proteins, regulating active zone scaffold proteins, fusion machinery proteins, motor proteins, endocytic proteins, several enzymes, and even Ca2+ channels, following the decay of Ca2+ concentration after the action potential. Here, I summarize the Ca2+-dependent protein controls of synchronous and asynchronous vesicle release, rapid replenishment of the active zone, endocytosis, and short-term plasticity within 100 msec after the action potential. Furthermore, I discuss the contribution of active zone proteins to presynaptic plasticity and to homeostatic readjustment during and after intense activity, in addition to activity-dependent endocytosis. Full article
(This article belongs to the Special Issue News about Structure and Function of Synapses: Health and Diseases)
►▼ Show Figures

Figure 1

20 pages, 1867 KiB  
Review
NMDA and AMPA Receptors at Synapses: Novel Targets for Tau and α-Synuclein Proteinopathies
by Maria Italia, Elena Ferrari, Monica Diluca and Fabrizio Gardoni
Biomedicines 2022, 10(7), 1550; https://doi.org/10.3390/biomedicines10071550 - 29 Jun 2022
Cited by 6 | Viewed by 2504
Abstract
A prominent feature of neurodegenerative diseases is synaptic dysfunction and spine loss as early signs of neurodegeneration. In this context, accumulation of misfolded proteins has been identified as one of the most common causes driving synaptic toxicity at excitatory glutamatergic synapses. In particular, [...] Read more.
A prominent feature of neurodegenerative diseases is synaptic dysfunction and spine loss as early signs of neurodegeneration. In this context, accumulation of misfolded proteins has been identified as one of the most common causes driving synaptic toxicity at excitatory glutamatergic synapses. In particular, a great effort has been placed on dissecting the interplay between the toxic deposition of misfolded proteins and synaptic defects, looking for a possible causal relationship between them. Several studies have demonstrated that misfolded proteins could directly exert negative effects on synaptic compartments, altering either the function or the composition of pre- and post-synaptic receptors. In this review, we focused on the physiopathological role of tau and α-synuclein at the level of postsynaptic glutamate receptors. Tau is a microtubule-associated protein mainly expressed by central nervous system neurons where it exerts several physiological functions. In some cases, it undergoes aberrant post-translational modifications, including hyperphosphorylation, leading to loss of function and toxic aggregate formation. Similarly, aggregated species of the presynaptic protein α-synuclein play a key role in synucleinopathies, a group of neurological conditions that includes Parkinson’s disease. Here, we discussed how tau and α-synuclein target the postsynaptic compartment of excitatory synapses and, specifically, AMPA- and NMDA-type glutamate receptors. Notably, recent studies have reported their direct functional interactions with these receptors, which in turn could contribute to the impaired glutamatergic transmission observed in many neurodegenerative diseases. Full article
(This article belongs to the Special Issue News about Structure and Function of Synapses: Health and Diseases)
►▼ Show Figures

Figure 1

Other

Jump to: Editorial, Review

9 pages, 1030 KiB  
Brief Report
Increased Extrasynaptic Glutamate Escape in Stochastically Shaped Probabilistic Synaptic Environment
by Leonid P. Savtchenko and Dmitri A. Rusakov
Biomedicines 2022, 10(10), 2406; https://doi.org/10.3390/biomedicines10102406 - 26 Sep 2022
Cited by 3 | Viewed by 1406
Abstract
Excitatory synapses in the brain are often surrounded by nanoscopic astroglial processes that express high-affinity glutamate transporters at a high surface density. This ensures that the bulk of glutamate leaving the synaptic cleft is taken up for its subsequent metabolic conversion and replenishment [...] Read more.
Excitatory synapses in the brain are often surrounded by nanoscopic astroglial processes that express high-affinity glutamate transporters at a high surface density. This ensures that the bulk of glutamate leaving the synaptic cleft is taken up for its subsequent metabolic conversion and replenishment in neurons. Furthermore, variations in the astroglial coverage of synapses can thus determine to what extent glutamate released into the synaptic cleft could activate its receptors outside the cleft. The biophysical determinants of extrasynaptic glutamate actions are complex because they involve a competition between transporters and target receptors of glutamate in the tortuous space of synaptic environment. To understand key spatiotemporal relationships between the extrasynaptic landscapes of bound and free glutamate, we explored a detailed Monte Carlo model for its release, diffusion, and uptake. We implemented a novel representation of brain neuropil in silico as a space filled with randomly scattered, overlapping spheres (spheroids) of distributed size. The parameters of perisynaptic space, astroglial presence, and glutamate transport were constrained by the empirical data obtained for the ‘average’ environment of common cortical synapses. Our simulations provide a glimpse of the perisynaptic concentration landscapes of free and transporter-bound glutamate relationship, suggesting a significant tail of space-average free glutamate within 3 ms post-release. Full article
(This article belongs to the Special Issue News about Structure and Function of Synapses: Health and Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop