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

机译:轴突可塑性支撑了颈椎病脊髓模型大鼠手术减压后的功能恢复

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摘要

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.
机译:颈椎病脊髓病(CSM)是最常见的脊髓疾病,是成年人残疾的主要原因。手术减压后的改善是有限的,患者通常仍然严重残疾。验尸研究表明,CSM与严重的轴突丢失有关。然而,我们对CSM病理生理学的了解仍然有限。为了研究关于轴突可塑性在手术减压后恢复中起作用的假设,我们采用了轻度至中度CSM的新型临床前模型。脊髓压迫导致明显的运动能力下降,轴突损伤标记APP的表达增加和血清素能纤维的丢失。手术减压可部分逆转缺陷并减弱APP表达。减压还与轴突发芽有关,反映在血清素能纤维的恢复和GAP43表达的增加上。突触素的重新表达表明减压后功能性突触的恢复。因此,促进轴突可塑性可能是促进CSM神经恢复的治疗策略。

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