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Advances in Synaptic Transmission and Plasticity
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Advances in Synaptic Transmission and Plasticity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 1737

Special Issue Editor

Dr. Manuela Dicarlo

E-Mail Website
Guest Editor
Department of Precision and Regenerative Medicine and Ionian Area (DiMePRe-J), University of Bari Aldo Moro, Piazza Giulio Cesare 11, 70124 Bari, Italy
Interests: neurodegenerative diseases; Alzheimer’s disease; depression; anxiety; memory; learning; ageing; neuroinflammation; neurotrophic factors; synaptic plasticity; cell biology; irisin; prefrontal cortex; hippocampus; histology; electron microscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Synaptic transmission is a fascinating biological event that allows neuronal communication with target cells via chemical mediators (i.e., neurotransmitters) or electric signals through gap junctions. The efficacy and strength of synaptic connections are finely tuned over time and the activity-dependent modifications in synaptic transmission, referred to as synaptic plasticity, involve a complex network of factors. Synaptic plasticity, first identified as a crucial mechanism for memory and learning, also plays pivotal roles in the early development of neural networks. In recent decades, accumulating evidence has emerged to support the hypothesis that alterations in synaptic plasticity mechanisms might contribute to prominent brain disorders, such as neurodegenerative and neuropsychiatric diseases. In this Special Issue, we invite authors to submit high-quality original research papers and review articles that shed light on new findings on the molecular and cellular mechanisms underlying synaptic transmission and plasticity processes in both healthy and pathological conditions through molecular biology, behavior, electrophysiology, and imaging approaches.

Dr. Manuela Dicarlo
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Keywords

  • synaptic transmission
  • synapse
  • neurotransmitters
  • synaptic plasticity
  • memory
  • learning
  • neurodegenerative diseases
  • neuropsychiatric diseases

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Published Papers (1 paper)

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Research

16 pages, 2747 KiB  
Article
A Novel 14mer Peptide Inhibits Autophagic Flux via Selective Activation of the mTORC1 Signalling Pathway: Implications for Alzheimer’s Disease
by Cloe García Porta, Kashif Mahfooz, Joanna Komorowska, Sara Garcia-Rates and Susan Greenfield
Int. J. Mol. Sci. 2024, 25(23), 12837; https://doi.org/10.3390/ijms252312837 - 29 Nov 2024
Viewed by 1164
Abstract
During development, a 14mer peptide, T14, modulates cell growth via the α-7 nicotinic acetylcholine receptor (α7 nAChR). However, this process could become excitotoxic in the context of the adult brain, leading to pathologies such as Alzheimer’s disease (AD). Recent work shows that T14 [...] Read more.
During development, a 14mer peptide, T14, modulates cell growth via the α-7 nicotinic acetylcholine receptor (α7 nAChR). However, this process could become excitotoxic in the context of the adult brain, leading to pathologies such as Alzheimer’s disease (AD). Recent work shows that T14 acts selectively via the mammalian target of rapamycin complex 1 (mTORC1). This pathway is essential for normal development but is overactive in AD. The triggering of mTORC1 has also been associated with the suppression of autophagy, commonly observed in ageing and neurodegeneration. We therefore investigated the relationship between T14 and autophagic flux in tissue cultures, mouse brain slices, and human Alzheimer’s disease hippocampus. Here, we demonstrate that T14 and p-mTOR s2448 expression significantly increases in AD human hippocampus, which was associated with the gradual decrease in the autophagosome number across Braak stages. During development, the reduction in T14 positively correlated with pTau (Ser202, Thr205) and two selective autophagy receptors: p62 and optineurin. In vitro studies also indicated that T14 increases p-mTOR s2448 expression, resulting in the aggregation of polyubiquinated substances. The effective blockade of T14 via its cyclic variant, NBP14, has been validated in vitro, in vivo, and ex vivo. In this study, NBP14 significantly attenuated p-mTOR s2448 expression and restored normal autophagic flux, as seen with rapamycin. We conclude that T14 acts at the α-7 receptor to selectively activate the mTORC1 pathway and consequently inhibit autophagic flux. Hence, this study describes a further step in the process by which T14 could drive neurodegeneration. Full article
(This article belongs to the Special Issue Advances in Synaptic Transmission and Plasticity)
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