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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 December 2025 | Viewed by 6838

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 (4 papers)

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Research

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17 pages, 1749 KB  
Article
Frequency-Dependent Modulation of Short-Term Neuronal Dynamics in the Female and Male Dorsal and Ventral Rat Hippocampus
by Athina Miliou, Giota Tsotsokou, Michaela Tsouka, Andriana Koutsoumpa and Costas Papatheodoropoulos
Int. J. Mol. Sci. 2025, 26(17), 8424; https://doi.org/10.3390/ijms26178424 - 29 Aug 2025
Viewed by 488
Abstract
Short-term synaptic plasticity (STSP) and short-term neuronal dynamics (STND) are fundamental properties of neural circuits, essential for information processing and brain function. Emerging evidence suggests that biological sex may influence these properties, yet sex-related differences in STSP and STND remain underexplored. This study [...] Read more.
Short-term synaptic plasticity (STSP) and short-term neuronal dynamics (STND) are fundamental properties of neural circuits, essential for information processing and brain function. Emerging evidence suggests that biological sex may influence these properties, yet sex-related differences in STSP and STND remain underexplored. This study investigates sex-specific differences in short-term synaptic plasticity (STSP) and neuronal dynamics (STND) along the dorsoventral axis of the rat hippocampus. Our findings reveal that both STSP and STND exhibit significant variation between female and male subjects. These differences are particularly pronounced in the ventral hippocampus, a region associated with affective and motivational processes. Given the role of short-term activity-dependent neuronal phenomena in modulating information processing and network function, these findings suggest potential functional implications for sex-specific cognitive and emotional regulation. The results highlight the importance of incorporating sex as a biological variable in studies of hippocampal physiology and its relation to behavior. Full article
(This article belongs to the Special Issue Advances in Synaptic Transmission and Plasticity)
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12 pages, 1017 KB  
Article
Forebrain-Specific B-raf Deficiency Reduces NMDA Current and Enhances Small-Conductance Ca2+-Activated K+ (SK) Current
by Cornelia Ruxanda, Christian Alzheimer and Fang Zheng
Int. J. Mol. Sci. 2025, 26(15), 7172; https://doi.org/10.3390/ijms26157172 - 25 Jul 2025
Viewed by 411
Abstract
B-raf (rapidly accelerated fibrosarcoma) is a crucial player within the ERK/MAPK signaling pathway. In the CNS, B-raf has been implicated in neuronal differentiation, long-term memory, and major depression. Mice with forebrain neuron-specific B-raf knockout show behavioral deficits in spatial learning tasks and impaired [...] Read more.
B-raf (rapidly accelerated fibrosarcoma) is a crucial player within the ERK/MAPK signaling pathway. In the CNS, B-raf has been implicated in neuronal differentiation, long-term memory, and major depression. Mice with forebrain neuron-specific B-raf knockout show behavioral deficits in spatial learning tasks and impaired hippocampal long-term potentiation (LTP). To elucidate the mechanism(s) underlying diminished synaptic plasticity in B-raf-deficient mice, we performed whole-cell recordings from CA1 pyramidal cells in hippocampal slices of control and B-raf mutant mice. We found that the NMDA/AMPA ratio of excitatory postsynaptic currents (EPSCs) at the Schaffer collateral—CA1 pyramidal cell synapses was significantly reduced in B-raf mutants, which would at least partially account for their impaired LTP. Interestingly, the reduced NMDA component of field postsynaptic potentials in mutant preparations was partially reinstated by blocking the apamin-sensitive small-conductance Ca2+-activated K+ (SK) channels, which have also been reported to modulate hippocampal LTP and learning tasks. To determine the impact of B-raf-dependent signaling on SK current, we isolated the apamin-sensitive tail current after a strong depolarizing event and found indeed a significantly bigger SK current in B-raf-deficient cells compared to controls, which is consistent with the reduced action potential firing and the stronger facilitating effect of apamin on CA1 somatic excitability in B-raf-mutant hippocampus. Our data suggest that B-raf signaling readjusts the delicate balance between NMDA receptors and SK channels to promote synaptic plasticity and facilitate hippocampal learning and memory. Full article
(This article belongs to the Special Issue Advances in Synaptic Transmission and Plasticity)
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16 pages, 2747 KB  
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 1862
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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Review

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20 pages, 4246 KB  
Review
Hydrogen Sulfide (H2S- or H2Sn-Polysulfides) in Synaptic Plasticity: Modulation of NMDA Receptors and Neurotransmitter Release in Learning and Memory
by Constantin Munteanu, Anca Irina Galaction, Gelu Onose, Marius Turnea and Mariana Rotariu
Int. J. Mol. Sci. 2025, 26(7), 3131; https://doi.org/10.3390/ijms26073131 - 28 Mar 2025
Cited by 1 | Viewed by 2853
Abstract
Hydrogen sulfide (H2S) has emerged as a pivotal gaseous transmitter in the central nervous system, influencing synaptic plasticity, learning, and memory by modulating various molecular pathways. This review examines recent evidence regarding how H2S regulates NMDA receptor function and [...] Read more.
Hydrogen sulfide (H2S) has emerged as a pivotal gaseous transmitter in the central nervous system, influencing synaptic plasticity, learning, and memory by modulating various molecular pathways. This review examines recent evidence regarding how H2S regulates NMDA receptor function and neurotransmitter release in neuronal circuits. By synthesizing findings from animal and cellular models, we investigate the impacts of enzymatic H2S production and exogenous H2S on excitatory synaptic currents, long-term potentiation, and intracellular calcium signaling. Data suggest that H2S interacts directly with NMDA receptor subunits, altering receptor function and modulating neuronal excitability. Simultaneously, H2S promotes the release of neurotransmitters such as glutamate and GABA, shaping synaptic dynamics and plasticity. Furthermore, reports indicate that disruptions in H2S metabolism contribute to cognitive impairments and neurodegenerative disorders, underscoring the potential therapeutic value of targeting H2S-mediated pathways. Although the precise mechanisms of H2S-induced changes in synaptic strength remain elusive, a growing body of evidence positions H2S as a significant regulator of memory formation processes. This review calls for more rigorous exploration into the molecular underpinnings of H2S in synaptic plasticity, paving the way for novel pharmacological interventions in cognitive dysfunction. Full article
(This article belongs to the Special Issue Advances in Synaptic Transmission and Plasticity)
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