Chemorepellent Axon Guidance Molecules in Spinal Cord Injury

2006 ◽  
Vol 23 (3-4) ◽  
pp. 409-421 ◽  
Author(s):  
Simone P. Niclou ◽  
Erich M.E. Ehlert ◽  
Joost Verhaagen
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axon Guidance ◽  
Cord Injury ◽  
Guidance Molecules

scholarly journals Olig2-Induced Semaphorin Expression Drives Corticospinal Axon Retraction After Spinal Cord Injury

2020 ◽  
Vol 30 (11) ◽  
pp. 5702-5716
Author(s):  
Masaki Ueno ◽  
Yuka Nakamura ◽  
Hiroshi Nakagawa ◽  
Jesse K Niehaus ◽  
Mari Maezawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axon Guidance ◽  
Conditional Deletion ◽  
Cord Injury ◽  
Axon Retraction ◽  
The Central Nervous System ◽  
Genetic Deletion ◽  
Putative Enhancer

Abstract Axon regeneration is limited in the central nervous system, which hinders the reconstruction of functional circuits following spinal cord injury (SCI). Although various extrinsic molecules to repel axons following SCI have been identified, the role of semaphorins, a major class of axon guidance molecules, has not been thoroughly explored. Here we show that expression of semaphorins, including Sema5a and Sema6d, is elevated after SCI, and genetic deletion of either molecule or their receptors (neuropilin1 and plexinA1, respectively) suppresses axon retraction or dieback in injured corticospinal neurons. We further show that Olig2+ cells are essential for SCI-induced semaphorin expression, and that Olig2 binds to putative enhancer regions of the semaphorin genes. Finally, conditional deletion of Olig2 in the spinal cord reduces the expression of semaphorins, alleviating the axon retraction. These results demonstrate that semaphorins function as axon repellents following SCI, and reveal a novel transcriptional mechanism for controlling semaphorin levels around injured neurons to create zones hostile to axon regrowth.

scholarly journals Targeting axon guidance cues for neural circuit repair after spinal cord injury

2020 ◽  
pp. 0271678X2096185
Author(s):  
Yimin Zou
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axon Guidance ◽  
Spinal Cord Injuries ◽  
Neural Circuit ◽  
Functional Restoration ◽  
Spinal Cord Tissue ◽  
Cord Injury ◽  
The Many

At least two-thirds of spinal cord injury cases are anatomically incomplete, without complete spinal cord transection, although the initial injuries cause complete loss of sensory and motor functions. The malleability of neural circuits and networks allows varied extend of functional restoration in some individuals after successful rehabilitative training. However, in most cases, the efficiency and extent are both limited and uncertain, largely due to the many obstacles of repair. The restoration of function after anatomically incomplete injury is in part made possible by the growth of new axons or new axon branches through the spared spinal cord tissue and the new synaptic connections they make, either along the areas they grow through or in the areas they terminate. This review will discuss new progress on the understanding of the role of axon guidance molecules, particularly the Wnt family proteins, in spinal cord injury and how the knowledge and tools of axon guidance can be applied to increase the potential of recovery. These strategies, combined with others, such as neuroprotection and rehabilitation, may bring new promises. The recovery strategies for anatomically incomplete spinal cord injuries are relevant and may be applicable to traumatic brain injury and stroke.

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