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Plasticity of the Nervous System after Injury: 2nd Edition
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Plasticity of the Nervous System after Injury: 2nd Edition

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: 20 April 2025 | Viewed by 2408

Special Issue Editors

Prof. Dr. Xavier Navarro

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Guest Editor
Instituto de Neurociencias, Universitat Autònoma de Barcelona, Cerdanyola del Valles, Spain
Interests: nerve injuries; regeneration; neural plasticity; axonal regeneration
Prof. Dr. Tessa Gordon

E-Mail Website
Guest Editor
Department of Surgery, Division of Plastic Reconstructive Surgery, 06.9706 Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada
Interests: nerve injuries; regeneration; neural plasticity; axonal regeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Functional recovery is too often poor after peripheral nerve injuries. This is in spite of the capacity of supporting glial cells, the Schwann cells that myelinate the axons, to support the regeneration of the injured axons and to reinnervate their target muscle and sense organs. Recovery of function is even more severely limited in the central nervous system. This is due to the inability of the glial cells, oligodendrocytes, to support the growth of central axons. Studies regarding peripheral nerve injuries are revealing recovery mechanisms and novel methodologies to promote functional motor and sensory recovery. These include the activation of intrinsic growth pathways, as well as the use of brief low-frequency electrical stimulation, intermittent hypoxia, bioluminescent optogenetics, optimized nerve grafts and nerve transfers, stem cells, and manufactured Schwann cells for nerve repair. The dynamics of plasticity after spinal cord injuries and the relevance of locomotor networks in restoring function provide a means to restore function after central nerve injuries.

Prof. Dr. Xavier Navarro
Prof. Dr. Tessa Gordon
Guest Editors

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

  • neural plasticity
  • axonal regeneration
  • nerve injury
  • glial cells
  • central nervous system

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Published Papers (2 papers)

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18 pages, 3790 KiB  
Article
Limited Nerve Regeneration across Acellular Nerve Allografts (ANAs) Coincides with Changes in Blood Vessel Morphology and the Development of a Pro-Inflammatory Microenvironment
by Jesús A. Acevedo Cintrón, Daniel A. Hunter, Lauren Schellhardt, Deng Pan, Susan E. Mackinnon and Matthew D. Wood
Int. J. Mol. Sci. 2024, 25(12), 6413; https://doi.org/10.3390/ijms25126413 - 11 Jun 2024
Cited by 1 | Viewed by 832
Abstract
The use of acellular nerve allografts (ANAs) to reconstruct long nerve gaps (>3 cm) is associated with limited axon regeneration. To understand why ANA length might limit regeneration, we focused on identifying differences in the regenerative and vascular microenvironment that develop within ANAs [...] Read more.
The use of acellular nerve allografts (ANAs) to reconstruct long nerve gaps (>3 cm) is associated with limited axon regeneration. To understand why ANA length might limit regeneration, we focused on identifying differences in the regenerative and vascular microenvironment that develop within ANAs based on their length. A rat sciatic nerve gap model was repaired with either short (2 cm) or long (4 cm) ANAs, and histomorphometry was used to measure myelinated axon regeneration and blood vessel morphology at various timepoints (2-, 4- and 8-weeks). Both groups demonstrated robust axonal regeneration within the proximal graft region, which continued across the mid-distal graft of short ANAs as time progressed. By 8 weeks, long ANAs had limited regeneration across the ANA and into the distal nerve (98 vs. 7583 axons in short ANAs). Interestingly, blood vessels within the mid-distal graft of long ANAs underwent morphological changes characteristic of an inflammatory pathology by 8 weeks post surgery. Gene expression analysis revealed an increased expression of pro-inflammatory cytokines within the mid-distal graft region of long vs. short ANAs, which coincided with pathological changes in blood vessels. Our data show evidence of limited axonal regeneration and the development of a pro-inflammatory environment within long ANAs. Full article
(This article belongs to the Special Issue Plasticity of the Nervous System after Injury: 2nd Edition)
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16 pages, 3703 KiB  
Article
Link Protein 1 Is Involved in the Activity-Dependent Modulation of Perineuronal Nets in the Spinal Cord
by Judith Sánchez-Ventura, Natalia Lago, Clara Penas, Xavier Navarro and Esther Udina
Int. J. Mol. Sci. 2024, 25(8), 4267; https://doi.org/10.3390/ijms25084267 - 12 Apr 2024
Viewed by 1066
Abstract
One of the challenges of the mature nervous system is to maintain the stability of neural networks while providing a degree of plasticity to generate experience-dependent modifications. This plasticity–stability dynamism is regulated by perineuronal nets (PNNs) and is crucial for the proper functioning [...] Read more.
One of the challenges of the mature nervous system is to maintain the stability of neural networks while providing a degree of plasticity to generate experience-dependent modifications. This plasticity–stability dynamism is regulated by perineuronal nets (PNNs) and is crucial for the proper functioning of the system. Previously, we found a relation between spinal PNNs reduction and maladaptive plasticity after spinal cord injury (SCI), which was attenuated by maintaining PNNs with activity-dependent therapies. Moreover, transgenic mice lacking the cartilage link protein 1 (Crtl1 KO mice) showed aberrant spinal PNNs and increased spinal plasticity. Therefore, the aim of this study is to evaluate the role of link protein 1 in the activity-dependent modulation of spinal PNNs surrounding motoneurons and its impact on the maladaptive plasticity observed following SCI. We first studied the activity-dependent modulation of spinal PNNs using a voluntary wheel-running protocol. This training protocol increased spinal PNNs in WT mice but did not modify PNN components in Crtl1 KO mice, suggesting that link protein 1 mediates the activity-dependent modulation of PNNs. Secondly, a thoracic SCI was performed, and functional outcomes were evaluated for 35 days. Interestingly, hyperreflexia and hyperalgesia found at the end of the experiment in WT-injured mice were already present at basal levels in Crtl1 KO mice and remained unchanged after the injury. These findings demonstrated that link protein 1 plays a dual role in the correct formation and in activity-dependent modulation of PNNs, turning it into an essential element for the proper function of PNN in spinal circuits. Full article
(This article belongs to the Special Issue Plasticity of the Nervous System after Injury: 2nd Edition)
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