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25th Anniversary of IJMS: Updates and Advances in Molecular Neurobiology

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: 31 December 2025 | Viewed by 51

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College of Medicine, University of Central Florida, Orlando, FL 32816, USA
Interests: stem cell; Alzheimer’s disease; neurodegenerative diseases; down syndrome; regeneration therapy; cancer stem cell; exosome
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Special Issue Information

Dear Colleagues,

The field of molecular neurobiology has undergone a remarkable transformation over the past 25 years, driven by rapid technological advances and deepening insights into the fundamental mechanisms governing brain development, function, and disease. In celebration of the 25th anniversary of the International Journal of Molecular Sciences (IJMS), this Special Issue, “25th Anniversary of IJMS: Updates and Advances in Molecular Neurobiology”, aims to highlight the latest developments, unresolved questions, and future directions in this dynamic and interdisciplinary area of research.

We welcome contributions that explore molecular and cellular processes underlying neural function and dysfunction. Topics of interest include but are not limited to the following: intracellular and intercellular signaling in neurons and glia, transcriptional and epigenetic regulation of neural gene expression, mechanisms of synaptic plasticity, protein misfolding and aggregation, neuroinflammatory cascades, and cell death pathways in neurodegenerative conditions. Additionally, we encourage submissions addressing the roles of non-coding RNAs, exosomes, ion channels, mitochondrial dysfunction, and the molecular basis of neuron–glia interactions.

This Special Issue also welcomes advances in cutting-edge methodologies—such as single-cell omics, CRISPR-based genome editing, optogenetics, and molecular imaging techniques—that provide new windows into the complexity of the nervous system at molecular resolution. Furthermore, we encourage translational studies that bridge molecular mechanisms with clinical applications, including biomarker discovery, drug development, and therapeutic strategies for neurodegenerative and neurodevelopmental disorders.

As we reflect on the progress made since the founding of IJMS, we look forward to contributions that not only celebrate past achievements but also illuminate emerging trends and critical challenges in molecular neurobiology. We invite researchers from basic science, clinical neuroscience, bioengineering, and related fields to join us in marking this milestone and shaping the future of brain research.

Prof. Dr. Kiminobu Sugaya
Guest Editor

Manuscript Submission Information

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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.

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Keywords

  • molecular neurobiology
  • neural signaling and gene regulation
  • synaptic plasticity
  • neurodevelopment
  • neurodegeneration
  • neuroregeneration
  • neuroinflammation
  • epigenetics in neuroscience
  • non-coding RNAs
  • protein misfolding and aggregation
  • exosomes and extracellular vesicles
  • stem cells and neural repair
  • biomarkers of neurological disease
  • translational neuroscience
  • neuropharmacology
  • brain omics (genomics, proteomics, transcriptomics)
  • neuronal-glial interactions
  • mitochondrial dysfunction in the nervous system

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Published Papers (1 paper)

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Research

17 pages, 3248 KiB  
Article
Interneuron-Driven Ictogenesis in the 4-Aminopyridine Model: Depolarization Block and Potassium Accumulation Initiate Seizure-like Activity
by Elena Yu. Proskurina, Julia L. Ergina and Aleksey V. Zaitsev
Int. J. Mol. Sci. 2025, 26(14), 6812; https://doi.org/10.3390/ijms26146812 - 16 Jul 2025
Abstract
The mechanisms of ictal discharge initiation remain incompletely understood, particularly the paradoxical role of inhibitory fast-spiking interneurons in seizure generation. Using simultaneous whole-cell recordings of interneurons and pyramidal neurons combined with extracellular [K+]o monitoring in mouse entorhinal cortex-hippocampal slices (4-aminopyridine [...] Read more.
The mechanisms of ictal discharge initiation remain incompletely understood, particularly the paradoxical role of inhibitory fast-spiking interneurons in seizure generation. Using simultaneous whole-cell recordings of interneurons and pyramidal neurons combined with extracellular [K+]o monitoring in mouse entorhinal cortex-hippocampal slices (4-aminopyridine model of epileptiform activity), we identified a critical transition sequence: interneurons displayed high-frequency firing during the preictal phase before entering depolarization block (DB). DB onset coincided with the peak of rate of extracellular [K+] accumulation. Pyramidal cells remained largely silent during interneuronal hyperactivity but started firing within 1.1 ± 0.3 s after DB onset, marking the transition to ictal discharges. This consistent sequence (interneuron DB → [K+]o rate peak → pyramidal cell firing) was observed in 100% of entorhinal cortex recordings. Importantly, while neurons across all entorhinal cortical layers synchronously fired during the first ictal discharge, hippocampal CA1 neurons showed fundamentally different activity: they generated high-frequency interictal bursts but did not participate in ictal events, indicating region-specific seizure initiation mechanisms. Our results demonstrate that interneuron depolarization block acts as a precise temporal switch for ictogenesis and suggest that the combined effect of disinhibition and K+-mediated depolarization triggers synchronous pyramidal neuron recruitment. These findings provide a mechanistic framework for seizure initiation in focal epilepsy, highlighting fast-spiking interneurons dysfunction as a potential therapeutic target. Full article
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