Axonal plasticity underpins the functional recovery following surgical decompression in a rat model of cervical spondylotic myelopathy

Cervical spondylotic myelopathy (CSM) is the most common spinal cord disorder and a major cause of disability in adults. Improvements following surgical decompression are limited and patients often remain severely disabled. Post mortem studies indicate that CSM is associated with profound axonal los...

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Bibliographic Details
Published in:Acta neuropathologica communications 2016-08, Vol.4 (1), p.89, Article 89
Main Authors: Dhillon, Rana S, Parker, John, Syed, Yasir A, Edgley, Steve, Young, Adam, Fawcett, James W, Jeffery, Nick D, Franklin, Robin J M, Kotter, Mark R N
Format: Article
Language:English
Subjects:
Animals
Apoptosis - physiology
Axons - pathology
Axons - physiology
Decompression, Surgical
Disease Models, Animal
Immunohistochemistry
Male
Motor Activity - physiology
Neuroglia - pathology
Neuroglia - physiology
Neuronal Plasticity - physiology
Random Allocation
Rats, Sprague-Dawley
Recovery of Function - physiology
Severity of Illness Index
Spinal Cord Compression - pathology
Spinal Cord Compression - physiopathology
Spinal Cord Compression - surgery
Spondylosis - pathology
Spondylosis - physiopathology
Spondylosis - surgery
Surgery
Synapses - pathology
Synapses - physiology
Synaptophysin - metabolism
Treatment Outcome
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Summary:Cervical spondylotic myelopathy (CSM) is the most common spinal cord disorder and a major cause of disability in adults. Improvements following surgical decompression are limited and patients often remain severely disabled. Post mortem studies indicate that CSM is associated with profound axonal loss. However, our understanding of the pathophysiology of CSM remains limited.To investigate the hypothesis that axonal plasticity plays a role in the recovery following surgical decompression, we adopted a novel preclinical model of mild to moderate CSM. Spinal cord compression resulted in significant locomotor deterioration, increased expression of the axonal injury marker APP, and loss of serotonergic fibres. Surgical decompression partially reversed the deficits and attenuated APP expression. Decompression was also associated with axonal sprouting, reflected in the restoration of serotonergic fibres and an increase of GAP43 expression. The re-expression of synaptophysin indicated the restoration of functional synapses following decompression. Promoting axonal plasticity may therefore be a therapeutic strategy for promoting neurological recovery in CSM.
ISSN:2051-5960
2051-5960
DOI:10.1186/s40478-016-0359-7