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首页> 外文期刊>Progress in brain research >Segmental organization of spinal reflexes mediating autonomic dysreflexia after spinal cord injury.
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Segmental organization of spinal reflexes mediating autonomic dysreflexia after spinal cord injury.

机译：脊髓反射的节段性组织介导了脊髓损伤后的自主神经反射异常。

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Spinal cord injuries above mid-thoracic levels can lead to a potentially life-threatening hypertensive condition termed autonomic dysreflexia that is often triggered by distension of pelvic viscera (bladder or bowel). This syndrome is characterized by episodic hypertension due to sudden, massive discharge of sympathetic preganglionic neurons in the thoracolumbar spinal cord. This hypertension is usually accompanied by bradycardia, particularly if the injury is caudal to the 2nd to 4th thoracic spinal segments. The development of autonomic dysreflexia is correlated with aberrant sprouting of peptidergic afferent fibers into the spinal cord below the injury. In particular, sprouting of nerve growth factor-responsive afferent fibers has been shown to have a major influence on dysreflexia, perhaps by amplifying the activation of disinhibited sympathetic neurons. Using a model of noxious bowel distension after complete thoracic spinal transection at the 4th thoracic segment in rats, we selectively altered C-fiber sprouting, at specified spinal levels caudal to the injury, with microinjections of adenovirus encoding the growth-promoting nerve growth factor or the growth-inhibitory semaphorin 3A. This was followed by assessment of physiological responses to colorectal distension and subsequent histology. Additionally, anterograde tract tracers were injected into the lumbosacral region to compare the extent of labeled propriospinal rostral projections in uninjured cords to those in cords after complete 4th thoracic transection. In summary, overexpression of chemorepulsive semaphorin 3A impeded C-fiber sprouting in lumbosacral segments and mitigated hypertensive autonomic dysreflexia, whereas the opposite results were obtained with nerve growth factor overexpression. Furthermore, compared to naive rats, there were significantly more labeled lumbosacral propriospinal projections rostrally after thoracic injury. Collectively, our findings suggest that distension of pelvic viscera increases the excitation of expandedafferent terminals in the disinhibited lumbosacral spinal cord. This, in turn, triggers excitation and sprouting of local propriospinal neurons to relay visceral sensory stimuli and amplify the activation of sympathetic preganglionic neurons in the thoracolumbar cord, to enhance transmission in the spinal viscero-sympathetic reflex pathway. These responses are manifested as autonomic dysreflexia.
机译：胸中水平以上的脊髓损伤可导致潜在的危及生命的高血压病，称为自主神经反射异常，通常由盆腔内脏（膀胱或肠）扩张引起。该综合征的特征是由于胸腰椎脊髓中交感神经节前神经元突然大量放电而引起发作性高血压。这种高血压通常伴有心动过缓，尤其是在第二至第四胸椎节段尾部受伤的情况下。自主神经反射不良的发展与损伤以下的肽能传入纤维异常萌芽进入脊髓有关。特别是，神经生长因子反应性传入纤维的萌发已显示出对反射障碍的重要影响，也许是通过放大被抑制的交感神经元的激活来实现的。使用大鼠第4个胸段完全胸段脊髓横断后有害的肠扩张模型，我们通过显微注射编码促进生长的神经生长因子或抑制生长的信号量3A。随后评估对大肠扩张的生理反应和随后的组织学。另外，将顺行示踪剂注入腰s区域，以比较未受伤的脐带与完全第四次胸廓横切后的脐带中标记的脊柱前凸状突起的程度。总之，化学驱动信号蛋白3A的过表达阻碍了腰imp部C纤维的发芽并减轻了高血压的自主神经反射障碍，而神经生长因子的过表达则获得了相反的结果。此外，与幼稚大鼠相比，胸腔损伤后腰ro部脊柱脊柱前突明显更多。总的来说，我们的研究结果表明，盆腔内脏的扩张会增加腰部ac腰脊髓中扩张的末端的兴奋性。反过来，这会触发局部脊椎神经元的激发和萌发，以传递内脏感觉刺激并放大胸腰带中交感神经节前神经元的激活，从而增强脊髓内脏交感神经反射途径的传递。这些反应表现为自主神经反射不良。

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