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Brain Sciences
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How to Rewire the Brain—Neuroplasticity
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How to Rewire the Brain—Neuroplasticity

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 1849

Special Issue Editors

Dr. Jianyang Du

E-Mail Website
Guest Editor
Department of Anatomy and Neurobiology, The University of Tennessee Health Science Center, Memphis, TN 38163, USA
Interests: neural circuit; mouse behavior; psychiatric disorders; synaptic transmission and plasticity; learning and memory
Special Issues, Collections and Topics in MDPI journals
Dr. Hui Lu

E-Mail Website
Guest Editor
Department of Pharmacology and Physiology, School of Medicine and Health Sciences, The George Washington University, Washington, DC 20037, USA
Interests: machine learning; neural circuit coding of behavior; neural ensemble activity; neurological disorders; system neuroscience
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We would like to welcome you to this Special Issue of our scientific journal, dedicated to exploring the intricate world of brain circuits and neuroplasticity. Neuroplasticity, the brain's remarkable ability to reorganize itself in response to experiences, learning, and injury, is a cornerstone of neuroscience research. This Special Issue, titled “How to Rewire the Brain—Neuroplasticity”, explores the dynamic processes underpinning neural adaptation and their profound implications for cognition, behavior, and recovery from neurological disorders.

Through cutting-edge studies, we delve into the molecular, cellular, and systemic mechanisms that drive plasticity, from synaptic remodeling to large-scale network reorganization. Our contributors investigate how factors such as age, environment, and genetics influence plasticity and how these insights inform innovative therapeutic strategies, including neurorehabilitation, brain stimulation, and pharmacological interventions.

By unraveling the complexities of neuroplasticity, this Special Issue seeks to bridge foundational science with translational applications, offering new perspectives on how we can harness the brain’s adaptability to optimize health and function. We invite readers to explore these advances and their transformative potential. 

Dr. Jianyang Du
Dr. Hui Lu
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 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. Brain Sciences 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 2200 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

  • brain circuits
  • neural networks
  • synaptic plasticity
  • neural development
  • network dynamics
  • neural coding
  • information processing
  • neuron–glia interaction
  • behavioral output
  • neurological disorders

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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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17 pages, 2085 KiB  
Article
Chronic Fluoxetine Treatment Desensitizes Serotoninergic Inhibition of GABAergic Inputs and Intrinsic Excitability of Dorsal Raphe Serotonin Neurons
by Wei Zhang, Ying Jin and Fu-Ming Zhou
Brain Sci. 2025, 15(4), 384; https://doi.org/10.3390/brainsci15040384 - 8 Apr 2025
Viewed by 413
Abstract
Background: Dorsal raphe serotonin (5-hydroxytryptamine, 5-HT) neurons are spontaneously active and release 5-HT that is critical for normal brain function and regulates mood and emotion. Serotonin reuptake inhibitors (SSRIs) increase the synaptic and extracellular 5-HT level and are effective in treating depression. Treatment [...] Read more.
Background: Dorsal raphe serotonin (5-hydroxytryptamine, 5-HT) neurons are spontaneously active and release 5-HT that is critical for normal brain function and regulates mood and emotion. Serotonin reuptake inhibitors (SSRIs) increase the synaptic and extracellular 5-HT level and are effective in treating depression. Treatment of two weeks or longer is often required for SSRIs to produce clinical benefits. The cellular mechanism underlying this delay is not fully understood. Methods and Results: Using whole-cell patch clamp recording in brain slices, here we show that the GABAergic inputs inhibit the spike firing of raphe 5-HT neurons. This GABAergic regulation was reduced by 5-HT; additionally, this 5-HT effect was prevented by the G-protein-activated inwardly rectifying potassium (GirK) channel inhibitor tertiapin-Q, indicating a contribution of 5-HT activation of GirK channels in GABAergic presynaptic axon terminals. Equally important, after 14 days of treatment with fluoxetine, a widely used SSRI type antidepressant, the 5-HT inhibition of GABAergic inputs was downregulated. Furthermore, chronic fluoxetine treatment downregulated the 5-HT activation of the inhibitory GirK current in 5-HT neurons. Conclusions: Taken together, our results suggest that chronic fluoxetine treatment, by blocking 5-HT reuptake and hence increasing the extracellular 5-HT level, can downregulate the function of 5-HT1B receptors on the GABAergic afferent axon terminals synapsing onto 5-HT neurons, allowing extrinsic GABAergic neurons to more effectively influence 5-HT neurons; simultaneously, chronic fluoxetine treatment also downregulated somatic 5-HT autoreceptor-activated GirK channel-mediated hyperpolarization and decrease in input resistance, rendering 5-HT neurons resistant to autoinhibition and leading to increased 5-HT neuron activity. These neuroplastic changes in raphe 5-HT neurons and their GABAergic afferents may contribute to the behavioral effect of SSRIs. Full article
(This article belongs to the Special Issue How to Rewire the Brain—Neuroplasticity)
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11 pages, 2142 KiB  
Article
Dance Training and the Neuroplasticity of the Vestibular-Ocular Reflex: Preliminary Findings
by Raghav H. Jha, Erin G. Piker, Miranda Scalzo and Diana Trinidad
Brain Sci. 2025, 15(4), 355; https://doi.org/10.3390/brainsci15040355 - 29 Mar 2025
Viewed by 358
Abstract
Background: The impact of dance training on brainstem-mediated vestibular reflexes remains unclear. This study examined the vestibulo-ocular reflex (VOR) and its suppression during high-speed head movements, which may closely resemble the head-turning speeds used in dancers’ spotting techniques, using the video head impulse [...] Read more.
Background: The impact of dance training on brainstem-mediated vestibular reflexes remains unclear. This study examined the vestibulo-ocular reflex (VOR) and its suppression during high-speed head movements, which may closely resemble the head-turning speeds used in dancers’ spotting techniques, using the video head impulse test. Methods: Eighteen female college students (mean age: 21 years) were divided into two groups—nine trained dancers (≥six years of dance training) and nine age-matched non-dancers—all without a history of hearing, vestibular, or neurological disorders. VOR function was assessed using the head impulse paradigm (HIMP) and the suppression head impulse paradigm (SHIMP) for right and left lateral stimulation, with minimum head velocities of 150°/s. Results: All participants exhibited VOR measures within normal limits and the VOR gain of dancers did not significantly differ from that of non-dancers. However, most dancers reported a preference for right-sided pirouettes and the right-side SHIMP gain negatively correlated with years of training, suggesting a link between preferred turning direction and VOR suppression ability. Furthermore, dancers with over 15 years of training exhibited earlier anti-compensatory saccade latencies (~75 ms) during SHIMP. Conclusions: Trained dancers maintain a healthy VOR and may develop enhanced voluntary control, enabling more effective VOR suppression. The earlier onset of anti-compensatory saccades suggests neural adaptations in eye–head coordination for high-velocity movements. Given the study’s small sample size and the inclusion of non-fulltime dancers, future research with larger samples of professional dancers is needed for enhanced generalizability. These findings provide preliminary evidence of dance-related neuroplasticity in brainstem-mediated vestibular reflexes and open new research avenues. Full article
(This article belongs to the Special Issue How to Rewire the Brain—Neuroplasticity)
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Review

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21 pages, 1040 KiB  
Review
Neuroplasticity and Nervous System Recovery: Cellular Mechanisms, Therapeutic Advances, and Future Prospects
by Ligia Gabriela Tataranu and Radu Eugen Rizea
Brain Sci. 2025, 15(4), 400; https://doi.org/10.3390/brainsci15040400 - 15 Apr 2025
Viewed by 947
Abstract
Neuroplasticity, the ability of the nervous system to adapt structurally and functionally in response to environmental interactions and injuries, is a cornerstone of recovery in the central (CNS) and peripheral nervous systems (PNS). This review explores the mechanisms underlying neuroplasticity, focusing on the [...] Read more.
Neuroplasticity, the ability of the nervous system to adapt structurally and functionally in response to environmental interactions and injuries, is a cornerstone of recovery in the central (CNS) and peripheral nervous systems (PNS). This review explores the mechanisms underlying neuroplasticity, focusing on the dynamic roles of cellular and molecular processes in recovery from nervous system injuries. Key cellular players, including Schwann cells, oligodendrocytes, and neural stem cells, are highlighted for their contributions to nerve repair, myelination, and regeneration. Advances in therapeutic interventions, such as electrical stimulation, bioluminescent optogenetics, and innovative nerve grafting techniques, are discussed alongside their potential to enhance recovery and functional outcomes. The molecular underpinnings of plasticity, involving synaptic remodeling, homeostatic mechanisms, and activity-dependent regulation of gene expression, are elucidated to illustrate their role in learning, memory, and injury repair. Integrating emerging technologies and therapeutic approaches with a foundational understanding of neuroplasticity offers a pathway toward more effective strategies for restoring nervous system functionality after injury. Full article
(This article belongs to the Special Issue How to Rewire the Brain—Neuroplasticity)
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