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Biomedicines
Special Issues
Synaptic Function and Modulation in Health and Disease
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Synaptic Function and Modulation in Health and Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 3272

Special Issue Editor

Dr. Jean-Marie C. Bouteiller

E-Mail Website
Guest Editor
Center for Neural Engineering & Institute for Technology and Medical Systems Innovation, Alfred E. Mann Department of Biomedical Engineering, Viterbi School of Engineering & Keck School of Medicine, University of Southern California, Los Angeles, CA 90007, USA
Interests: hierarchical and temporal multiscale modeling of the nervous system; synaptic transmission; learning and memory; cognition in health and disease; therapeutics development; neuromodulation

Special Issue Information

Dear Colleagues,

Synaptic function and modulation are critical for proper nervous system function having been implicated in a myriad of processes ranging from basic neural communication to sophisticated behaviors and complex cognitive functions. Disruptions in synaptic mechanisms underlie a wide range of neurological and psychiatric disorders, highlighting it as a research area of the utmost importance to improve our understanding of these diseases and enable the development of more efficacious therapeutic strategies.

This Special Issue aims to gather recent developments in our understanding of synaptic function and modulation, emphasizing its roles in health and disease.

We encourage our colleagues to submit manuscripts on, but not limited to, the following topics: synaptic plasticity, neurotransmitter release, receptor dynamics, aging, and the impact of genetic and environmental factors on synaptic health. Computational studies are also welcome. By contributing to this Special Issue, authors will be able to share their research with a wide audience and thus foster collaboration and innovation in the field, thereby advancing our cumulative knowledge about this important topic.

Dr. Jean-Marie C. Bouteiller
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.

Keywords

  • synaptic function
  • synaptic plasticity
  • neurotransmitter release
  • receptor dynamics

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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14 pages, 1277 KiB  
Article
Experimentally Constrained Mechanistic and Data-Driven Models for Simulating NMDA Receptor Dynamics
by Duy-Tan J. Pham and Jean-Marie C. Bouteiller
Biomedicines 2025, 13(7), 1674; https://doi.org/10.3390/biomedicines13071674 - 8 Jul 2025
Viewed by 230
Abstract
Background: The N-methyl-d-aspartate receptor (NMDA-R) is a glutamate ionotropic receptor in the brain that is crucial for synaptic plasticity, which underlies learning and memory formation. Dysfunction of NMDA receptors is implicated in various neurological diseases due to their roles in both normal [...] Read more.
Background: The N-methyl-d-aspartate receptor (NMDA-R) is a glutamate ionotropic receptor in the brain that is crucial for synaptic plasticity, which underlies learning and memory formation. Dysfunction of NMDA receptors is implicated in various neurological diseases due to their roles in both normal cognition and excitotoxicity. However, their dynamics are challenging to capture accurately due to their high complexity and non-linear behavior. Methods: This article presents the elaboration and calibration of experimentally constrained computational models of GluN1/GluN2A NMDA-R dynamics: (1) a nine-state kinetic model optimized to replicate experimental data and (2) a computationally efficient look-up table model capable of replicating the dynamics of the nine-state kinetic model with a highly reduced footprint. Determination of the kinetic model’s parameter values was performed using the particle swarm optimization algorithm. The optimized kinetic model was then used to generate a rich input–output dataset to train the look-up table synapse model and estimate its coefficients. Results: Optimization produced a kinetic model capable of accurately reproducing experimentally found results such as frequency-dependent potentiation and the temporal response due to synaptic release of glutamate. Furthermore, the look-up table synapse model was able to closely mimic the dynamics of the optimized kinetic model. Conclusions: The results obtained with both models indicate that they constitute accurate alternatives for faithfully reproducing the dynamics of NMDA-Rs. High computational efficiency is also achieved with the use of the look-up table synapse model, making this implementation an ideal option for inclusion in large-scale neuronal models. Full article
(This article belongs to the Special Issue Synaptic Function and Modulation in Health and Disease)
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17 pages, 2482 KiB  
Article
Heterosynaptic Regulation of α2A-Adrenoceptors on Glutamate/GABA Release in the Prefrontal Cortex of Rats
by Yaru Wei, Yuhan Jiao, Xiaoting He, Xiaodong Tao, Baoming Li and Xuehan Zhang
Biomedicines 2025, 13(6), 1322; https://doi.org/10.3390/biomedicines13061322 - 28 May 2025
Viewed by 368
Abstract
Background/Objectives: Norepinephrine (NE) plays a crucial role in modulating cognitive processes via α2A-adrenoceptors (α2A-ARs) within the prefrontal cortex (PFC), an essential brain region responsible for higher cognitive functions. The α2A-ARs are found on both postsynaptic and presynaptic membranes in the PFC. Previous studies [...] Read more.
Background/Objectives: Norepinephrine (NE) plays a crucial role in modulating cognitive processes via α2A-adrenoceptors (α2A-ARs) within the prefrontal cortex (PFC), an essential brain region responsible for higher cognitive functions. The α2A-ARs are found on both postsynaptic and presynaptic membranes in the PFC. Previous studies have shown that presynaptic α2A-ARs, predominantly located at NE terminals, function as autoreceptors that inhibit NE release. However, the expression of α2A-ARs at non-NE terminals, such as glutamate and GABA, remains ambiguous. To clarify the expression patterns and potential roles of α2A-ARs at non-NE terminals, we investigated their presence at the axon terminals of excitatory glutamate neurons and inhibitory GABA neurons in the rat PFC using immunofluorescence double-labeling, whole-cell patch-clamp recordings, and pharmacological approaches. Methods: To clarify the expression patterns and potential roles of α2A-ARs at non-NE terminals, we investigated their presence at the axon terminals of glutamate neurons and GABA neurons in the rat PFC using immunofluorescence double-labeling, whole-cell patch-clamp recordings, and pharmacological approaches. Results: Our findings delineated the distribution of α2A-ARs at the axon terminals of both glutamate and GABA neurons, and the expression of α2A-AR in the pyramidal neurons within the rat PFC as well. Furthermore, we employed the selective α2A-AR agonist guanfacine to assess the functional role of presynaptic α2A-ARs at these non-NE terminals. Following the application of the PKA inhibitor PKI5–24 to block postsynaptic α2A-AR function, guanfacine still significantly decreased the frequency (not the amplitude) of miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) in layer 5–6 pyramidal neurons. Notably, the frequency reduction induced by guanfacine persisted even after the depletion of presynaptic NE vesicles. Conclusions: These findings offer a comprehensive analysis of presynaptic α2A-AR expression and function in the PFC, revealing for the first time their role as heteroreceptors that modulate the release of glutamate and GABA. Our results provide morphological and electrophysiological insights into a potential mechanism through which α2A-AR stimulation enhances cognitive functions. Full article
(This article belongs to the Special Issue Synaptic Function and Modulation in Health and Disease)
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Review

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22 pages, 2308 KiB  
Review
Stress-Induced Sleep Dysregulation: The Roles of Astrocytes and Microglia in Neurodegenerative and Psychiatric Disorders
by Ángel R. Rábago-Monzón, Juan F. Osuna-Ramos, David A. Armienta-Rojas, Josué Camberos-Barraza, Alejandro Camacho-Zamora, Javier A. Magaña-Gómez and Alberto K. De la Herrán-Arita
Biomedicines 2025, 13(5), 1121; https://doi.org/10.3390/biomedicines13051121 - 6 May 2025
Viewed by 2195
Abstract
Stress and sleep share a reciprocal relationship, where chronic stress often leads to sleep disturbances that worsen neurodegenerative and psychiatric conditions. Non-neuronal cells, particularly astrocytes and microglia, play critical roles in the brain’s response to stress and the regulation of sleep. Astrocytes influence [...] Read more.
Stress and sleep share a reciprocal relationship, where chronic stress often leads to sleep disturbances that worsen neurodegenerative and psychiatric conditions. Non-neuronal cells, particularly astrocytes and microglia, play critical roles in the brain’s response to stress and the regulation of sleep. Astrocytes influence sleep architecture by regulating adenosine signaling and glymphatic clearance, both of which can be disrupted by chronic stress, leading to reduced restorative sleep. Microglia, activated under stress conditions, drive neuroinflammatory processes that further impair sleep and exacerbate brain dysfunction. Additionally, the gut–brain axis mediates interactions between stress, sleep, and inflammation, with microbial metabolites influencing neural pathways. Many of these effects converge on the disruption of synaptic processes, such as neurotransmitter balance, synaptic plasticity, and pruning, which in turn contribute to the pathophysiology of neurodegenerative and psychiatric disorders. This review explores how these cellular and systemic mechanisms contribute to stress-induced sleep disturbances and their implications for neurodegenerative and psychiatric disorders, offering insights into potential therapeutic strategies targeting non-neuronal cells and the gut–brain axis. Full article
(This article belongs to the Special Issue Synaptic Function and Modulation in Health and Disease)
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