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Neural Networks in Molecular and Cellular Neurobiology

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 2669

Special Issue Editor

Special Issue Information

Dear Colleagues,

Neuronal networks are fundamental components of the nervous system, comprising tightly regulated molecular and cellular processes such as synaptic signaling, ion channel dynamics, and intracellular signaling cascades. Neural networks link gene expression, protein interactions, and intercellular communication to higher-order neural functions. Unraveling these mechanisms is a central challenge in molecular biology. Recent advances in molecular biology techniques, coupled with new tools such as machine learning and AI tools, are accelerating progress in this field.

This Special Issue will focus on cutting-edge research at the intersection of molecular neurobiology and neural networks, specifically examining the impact of molecular and cellular interactions on neural networks in health and disease. We welcome original research, reviews, case reports, and perspectives that provide new molecular insights into the organization, regulation, and dysfunction of neural networks.

Dr. Paschalis Theotokis
Guest Editor

Manuscript Submission Information

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Keywords

  • neural networks
  • neuroplasticity
  • intracellular signaling
  • computational neuroscience
  • artificial intelligence
  • neuromorphic computing

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Published Papers (2 papers)

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Research

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21 pages, 167029 KB  
Article
TGF-β1 Promotes the Recovery of Dorsal Root Ganglion Neurons from Cisplatin-Induced Injury Through Smad4-Dependent Mechanism
by Pan Wu, Yiling Wei, Xiang Chen, Qingmei Mo and Ming Zhuo
Curr. Issues Mol. Biol. 2026, 48(4), 344; https://doi.org/10.3390/cimb48040344 - 25 Mar 2026
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Abstract
Chemotherapy-induced peripheral (CIPN) neuropathy is a common dose-limiting side effect affecting roughly 30–40% patients. Dorsal root ganglia (DRG) neurons are one of the main targets of CIPN as chemotherapy drugs may accumulate in DRG neurons. Chemotherapy drugs may induce direct damages on DRG [...] Read more.
Chemotherapy-induced peripheral (CIPN) neuropathy is a common dose-limiting side effect affecting roughly 30–40% patients. Dorsal root ganglia (DRG) neurons are one of the main targets of CIPN as chemotherapy drugs may accumulate in DRG neurons. Chemotherapy drugs may induce direct damages on DRG neurons while also activating immune pathways, which results in the releasing of pro-inflammatory cytokines. This cascade may also damage neurons and amplify pain signaling. Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine with prominent immunomodulatory roles. Here, we report that TGF-β1 can promote axonal regeneration on DRG neurons injured by cisplatin via a suppressor of mothers against decapentaplegic (Smad) signaling pathway. To confirm the involvement of canonical TGF-β signaling, we applied the selective TGF-β type I receptor antagonist SB-431542 and performed a gene knockdown of Smad3 and Smad4, assessing their impacts on TGF-β1’s effects. Our results demonstrate that TGF-β1 could significantly enhance axonal regeneration in DRG, largely through a Smad4-dependent pathway, and we propose TGF-β1/Smad4 as a promising molecular target for treating CIPN. Full article
(This article belongs to the Special Issue Neural Networks in Molecular and Cellular Neurobiology)
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Review

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30 pages, 10570 KB  
Review
Molecular Physiology of the Neuronal Synapse
by María Jesús Ramírez-Expósito, Cristina Cueto-Ureña and José Manuel Martínez-Martos
Curr. Issues Mol. Biol. 2026, 48(1), 88; https://doi.org/10.3390/cimb48010088 - 15 Jan 2026
Cited by 1 | Viewed by 2035
Abstract
Neuronal synapses are the functional units of communication in the central nervous system. This review describes the molecular mechanisms regulating synaptic transmission, plasticity, and circuit refinement. At the presynaptic active zone, scaffolding proteins including bassoon, piccolo, RIMs, and munc13 organize vesicle priming and [...] Read more.
Neuronal synapses are the functional units of communication in the central nervous system. This review describes the molecular mechanisms regulating synaptic transmission, plasticity, and circuit refinement. At the presynaptic active zone, scaffolding proteins including bassoon, piccolo, RIMs, and munc13 organize vesicle priming and the localization of voltage-gated calcium channels. Neurotransmitter release is mediated by the SNARE complex, comprising syntaxin-1, SNAP25, and synaptobrevin, and triggered by the calcium sensor synaptotagmin-1. Following exocytosis, synaptic vesicles are recovered through clathrin-mediated, ultrafast, bulk, or kiss-and-run endocytic pathways. Postsynaptically, the postsynaptic density (PSD) serves as a protein hub where scaffolds such as PSD-95, shank, homer, and gephyrin anchor excitatory (AMPA, NMDA) and inhibitory (GABA-A, Glycine) receptors are observed. Synaptic strength is modified during long-term potentiation (LTP) and depression (LTD) through signaling cascades involving kinases like CaMKII, PKA, and PKC, or phosphatases such as PP1 and calcineurin. These pathways regulate receptor trafficking, Arc-mediated endocytosis, and actin-dependent remodeling of dendritic spines. Additionally, synapse formation and elimination are guided by cell adhesion molecules, including neurexins and neuroligins, and by microglial pruning via the complement cascade (C1q, C3) and “don’t eat me” signals like CD47. Molecular diversity is further expanded by alternative splicing and post-translational modifications. A unified model of synaptic homeostasis is required to understand the basis of neuropsychiatric and neurological disorders. Full article
(This article belongs to the Special Issue Neural Networks in Molecular and Cellular Neurobiology)
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