Morphological maladaptations in sympathetic preganglionic neurons following an experimental high-thoracic spinal cord injury.
Sachdeva R, Hutton G, Marwaha AS, Krassioukov AV
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.