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Biomolecules
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Regulation of Synapses in the Brain
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Regulation of Synapses in the Brain

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (17 July 2026) | Viewed by 2453

Editors

Prof. Dr. Kunwei Wu

E-Mail Website
Guest Editor
School of Anesthesiology, Xuzhou Medical University, Xuzhou, China
Interests: neuroscience; synapse; neural plasticity; cognition
Special Issues, Collections and Topics in MDPI journals
Dr. Guohao Wang

E-Mail Website
Co-Guest Editor
National Institute of Health, Bethesda, MD, USA
Interests: neuroscience; synapse; protein complexes; cognition

Special Issue Information

Dear Colleagues,

The regulation of synapses in the brain is a crucial area of research that underpins our understanding of various neurophysiological processes and neurological disorders. Synaptic plasticity, the ability of synapses to strengthen or weaken over time, is fundamental to learning, memory, and overall brain function. Dysregulation of synaptic mechanisms is implicated in numerous conditions, including neurodevelopmental disorders, schizophrenia, and neurodegenerative diseases.

This Special Issue emphasizes the importance of investigating synaptic regulation and its implications for brain health and disease. Recent advances in molecular and cellular techniques have shed light on the intricate processes that govern synaptic formation, maintenance, and elimination. Additionally, emerging evidence highlights the role of the surrounding glial cells and the extracellular matrix in modulating synaptic dynamics.

We invite contributions that explore various aspects of synaptic regulation, including, but not limited to, the following:

  • Molecular mechanisms of synaptic formation and maturation.
  • The role of synaptic plasticity in learning and memory.
  • Contributions of glial cells in synaptic modulation and support.
  • Impact of neuroinflammatory processes on synaptic integrity.
  • Implications of synaptic dysfunction in psychiatric disorders.
  • Novel therapeutic strategies targeting synaptic regulation in brain diseases.

By gathering diverse perspectives on these topics, we aim to enhance our understanding of synaptic regulation's role in brain function and its implications for therapeutic interventions.

We look forward to your valuable contributions.

Prof. Dr. Kunwei Wu
Dr. Guohao Wang
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules 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 2700 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 plasticity
  • neurodevelopmental disorders
  • glial cells
  • synaptic formation
  • learning and memory
  • neuroinflammation
  • neurodegenerative diseases
  • extracellular matrix
  • synaptic dysfunction
  • therapeutic interventions

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

Published Papers (2 papers)

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Research

23 pages, 4579 KB  
Article
Chemogenetic Activation of LC Noradrenergic Afferents Facilitates Cerebellar CF–PC LTD via Presynaptic α2A–AR/CDK5/PKA Signaling
by Xu-Dong Zhang, Ying-Han Xu, Wang-Tong Wu, Lang-Yue Zheng, Xin-Yi Xu, Chun-Ping Chu and De-Lai Qiu
Biomolecules 2026, 16(7), 1042; https://doi.org/10.3390/biom16071042 - 17 Jul 2026
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Abstract
Cerebellar climbing fiber–Purkinje cell (CF–PC) long-term depression (LTD) plays a critical role in motor learning and is modulated by locus coeruleus (LC) noradrenergic afferents via distinct adrenergic receptor (AR) subtypes. Nevertheless, the mechanisms underlying LC noradrenergic neuron-mediated regulation of CF–PC LTD remain poorly [...] Read more.
Cerebellar climbing fiber–Purkinje cell (CF–PC) long-term depression (LTD) plays a critical role in motor learning and is modulated by locus coeruleus (LC) noradrenergic afferents via distinct adrenergic receptor (AR) subtypes. Nevertheless, the mechanisms underlying LC noradrenergic neuron-mediated regulation of CF–PC LTD remain poorly understood. Here, we investigated the effects of chemogenetic activation of LC noradrenergic afferents on CF–PC LTD in cerebellar slices from dopamine β-hydroxylase (DBH)-Cre mice using electrophysiology, glutamate sensor imaging, immunofluorescence and pharmacological approaches. Tetanic stimulation (5 Hz) of CFs induced CF–PC LTD under control conditions, and this LTD was enhanced by chemogenetic activation of LC noradrenergic afferents. Blockade of group I metabotropic glutamate receptors (mGluR1) abolished LTD under control conditions, whereas chemogenetic activation of LC noradrenergic afferents triggered a novel form of CF–PC LTD accompanied by an increased N2/N1 ratio. With mGluR1 blocked, chemogenetic activation of LC noradrenergic afferents failed to trigger the novel CF–PC LTD following blockade of α2-AR or α2A-AR, but not α2B-AR or α2C-AR. Importantly, chemogenetic activation of LC noradrenergic afferents triggered LTD of glutamate fluorescence at CF terminals, which was abolished by blockade of α2-AR or α2A-AR, but not α2B-AR or α2C-AR. Notably, inhibition of either cyclin-dependent kinase 5 (CDK5) or presynaptic, but not postsynaptic, protein kinase A (PKA) completely abolished the CF–PC LTD triggered by chemogenetic activation of LC noradrenergic afferents in mouse cerebellar slices. Immunofluorescence results showed robust α2A-AR expression throughout the cerebellar molecular layer, with intense signals along PC dendrites and clear colocalization with vesicular glutamate transporter 2 (vGluT2) at cerebellar CF terminals. These results indicate that activation of LC noradrenergic afferents potentiates CF–PC LTD by triggering Glu-LTD at CF terminals through the α2A-AR/CDK5/PKA signaling cascade in the mouse cerebellar cortex. Full article
(This article belongs to the Special Issue Regulation of Synapses in the Brain)
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13 pages, 1498 KB  
Article
Regulatory Ouabain Action on Excitatory Transmission in Rat Hippocampus: Facilitation of Synaptic Responses and Weakening of LTP
by Yulia D. Stepanenko, Dmitry A. Sibarov and Sergei M. Antonov
Biomolecules 2025, 15(9), 1236; https://doi.org/10.3390/biom15091236 - 27 Aug 2025
Cited by 3 | Viewed by 1363
Abstract
Cardiotonic steroids (CTS), including the endogenous compound ouabain, modulate neuronal Na/K-ATPase (NKA) activity in a concentration-dependent manner, affecting neuronal survival and function. While high concentrations of ouabain are neurotoxic, endogenous levels of 0.1–1 nM exert neuroprotective effects and influence intracellular signaling. However, the [...] Read more.
Cardiotonic steroids (CTS), including the endogenous compound ouabain, modulate neuronal Na/K-ATPase (NKA) activity in a concentration-dependent manner, affecting neuronal survival and function. While high concentrations of ouabain are neurotoxic, endogenous levels of 0.1–1 nM exert neuroprotective effects and influence intracellular signaling. However, the effects of physiologically relevant ouabain concentrations on excitatory synaptic transmission remain unclear. In this study, we examined how 1 nM ouabain affects synaptic responses in rat hippocampal CA1 neurons. Using whole-cell patch-clamp recordings of evoked excitatory postsynaptic currents (EPSCs) and extracellular recordings of field excitatory postsynaptic potentials (fEPSPs), we found that ouabain enhances excitatory synaptic transmission, increasing EPSC amplitude and fEPSP slope by 35–50%. This effect was independent of NMDA receptor (NMDAR) activity. Ouabain reduced the magnitude of NMDAR-dependent long-term potentiation (LTP), but still augmented fEPSPs when applied after LTP induction. This implies separate additive mechanisms. These observations exhibit that ouabain, at concentrations corresponding to endogenous levels, facilitates basal excitatory synaptic transmission while partially suppressing LTP. We propose that ouabain exerts dual modulatory effects in hippocampal networks via distinct synaptic mechanisms. Full article
(This article belongs to the Special Issue Regulation of Synapses in the Brain)
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