Spinal cord injury (SCI) disrupts the supraspinal vasomotor pathways to sympathetic preganglionic neurons (SPNs) leading to impaired blood pressure (BP) control that often results in episodes of autonomic dysreflexia and orthostatic hypotension. The physiological cardiovascular consequences of SCI are largely attributed to the plastic changes in spinal SPNs induced by their partial deafferentation. While multiple studies have investigated the morphological changes in SPNs following SCI with contrasting reports. Here we investigated the morphological changes in SPNs rostral and caudal to a high thoracic (T3) SCI at 1-, 4- and 8-weeks post injury. SPNs were identified using Nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH- diaphorase) staining and were quantified for soma size and various dendritic measurements. We show that rostral to the lesion, soma size was increased at 1 week along with increased dendritic arbor. The total dendritic length was also increased at chronic stage (8 weeks post SCI). Caudal to the lesion, the soma size or dendritic lengths did not change with SCI. However, dendritic branching was enhanced within a week post SCI and remained elevated throughout the chronic stages. These findings demonstrate that SPNs undergo significant structural changes form sub-acute to chronic stages post-SCI that likely determines their functional consequences. These changes are discussed in context of physiological cardiovascular outcomes post-SCI.

中文翻译：

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实验性高胸脊髓损伤后交感神经节前神经元的形态适应不良。

脊髓损伤（SCI）破坏了通往交感神经节前神经元（SPNs）的脊髓上血管舒缩通路，导致血压（BP）控制受损，这通常导致自主神经反射不良和体位性低血压发作。SCI的生理心血管后果在很大程度上归因于脊髓SPN的部分脱除咖啡因引起的可塑性变化。多项研究调查了SCI后SPN的形态变化，并有相反的报道。在这里，我们调查了伤后1、4和8周，SPN的喙状和尾状到高胸（T3）SCI的形态变化。SPNs使用烟酰胺腺嘌呤二核苷酸磷酸氢递黄递酶（NADPH-diaphorase）染色进行鉴定，并针对体大小和各种树突测量进行定量。我们显示，到病变部位的延髓，躯体大小在1周时随树突状乔木的增加而增加。在慢性阶段（SCI后8周），总树突长度也增加了。脊髓尾部病变的体细胞大小或树突长度未随SCI改变。然而，树突状分支在脊髓损伤后一周内增强，并且在整个慢性阶段均保持升高。这些发现表明，SPN在SCI之后进入亚急性阶段，经历了重大的结构变化，这很可能决定了它们的功能后果。这些变化是在SCI后的生理性心血管结果的背景下讨论的。体细胞大小或树突长度未随SCI改变。然而，树突状分支在脊髓损伤后一周内增强，并且在整个慢性阶段均保持升高。这些发现表明，SPN在SCI之后进入亚急性阶段，经历了重大的结构变化，这可能决定了它们的功能后果。这些变化是在SCI后的生理性心血管结果的背景下讨论的。体细胞大小或树突长度未随SCI改变。但是，树突状分支在脊髓损伤后一周内增强，并且在整个慢性阶段均保持升高。这些发现表明，SPN在SCI之后进入亚急性阶段，经历了重大的结构变化，这很可能决定了它们的功能后果。这些变化是在SCI后的生理性心血管结果的背景下讨论的。