Targeting Neuromuscular Plasticity in Injury and Motoneuron Disease

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 15 June 2026 | Viewed by 1085

Special Issue Editor


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Guest Editor
Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy
Interests: neuroscience; neural plasticity; amyotrophic lateral sclerosis; spinal cord injury; motoneuron; regenerative medicine
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Special Issue Information

Dear Colleagues,

Plastic changes, such as synaptic plasticity, synaptogenesis, fiber sprouting, dendritic remodeling and metabolic changes, are typical events associated with activity-dependent modification of neural circuits, including those responsible for compensatory changes occurring after various injury events, including stroke or mechanical damage to the central nervous system. An increasing body of evidence suggests that neuroplasticity could also be responsible for compensatory attempts during the progression of neurodegenerative disorders, including motoneuron diseases. As a result, symptom onset usually occurs long after the initiation of neuronal degeneration.

Although these compensatory plastic changes are unable to halt disease progression or repair damaged tissues, they represent an important mechanism for further study, as well as a promising target of therapy approaches.

Focusing exclusively on basic research, this Special Issue invites contributions that utilise experimental models to explore the role of plasticity in spinal cord injury or motoneuron diseases. We are particularly interested in studies that elucidate the fundamental biological processes of pathogenesis and repair. Research articles and reviews with a strong emphasis on mechanistic discoveries are welcome.

Dr. Rosario Gulino
Guest Editor

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Keywords

  • neural plasticity
  • dendritic remodelling
  • axonal sprouting
  • metabolic changes
  • mitochondrial dysfunction
  • amyotrophic lateral sclerosis
  • motoneuron
  • spinal cord injury
  • regenerative medicine

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Published Papers (1 paper)

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Research

15 pages, 3805 KB  
Article
Effects of Clobetasol in an Aging Mouse Model of Spinal Cord Hemisection
by Maria Ciuro, Maria Sangiorgio, Giuliano Cantone, Carlo Fichera, Valeria Cacciato, Giampiero Leanza and Rosario Gulino
Biology 2025, 14(11), 1595; https://doi.org/10.3390/biology14111595 - 14 Nov 2025
Viewed by 762
Abstract
Spinal cord injury leads to permanent neurological deficits, and aging further diminishes the plasticity and regenerative responses required for recovery. Activation of the Sonic hedgehog (Shh) pathway through the receptor Smoothened (Smo) has been proposed as a potential strategy to promote repair, and [...] Read more.
Spinal cord injury leads to permanent neurological deficits, and aging further diminishes the plasticity and regenerative responses required for recovery. Activation of the Sonic hedgehog (Shh) pathway through the receptor Smoothened (Smo) has been proposed as a potential strategy to promote repair, and clobetasol, a potent glucocorticoid, has been identified as a pharmacological Smo agonist. However, the possible restorative effect of Smo agonists has never been studied during aging. Here, the effects of clobetasol treatment have been investigated in aging mice following spinal cord hemisection. Animals received weekly systemic injections of clobetasol or vehicle and were monitored for 11 weeks using the Basso Mouse Scale and open field test, followed by post-mortem histological analysis. Vehicle-treated mice exhibited a modest spontaneous recovery of locomotor function, whereas clobetasol-treated mice failed to improve and displayed significantly worse motor performance. Histological evaluation revealed reduced synaptic density in clobetasol-treated mice. Moreover, microglia/macrophage reaction was increased in vehicle-treated injured mice but suppressed by clobetasol, consistent with glucocorticoid-mediated inhibition of inflammatory responses. Together, these findings indicate that in aged animals clobetasol administration does not enhance plasticity or promote recovery but instead exacerbates synaptic loss and functional deficits. These results underscore the importance of age as a determinant of therapeutic efficacy after spinal cord injury. Full article
(This article belongs to the Special Issue Targeting Neuromuscular Plasticity in Injury and Motoneuron Disease)
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