Changes in the morphology of sympathetic preganglionic neurons parallel the development of autonomic dysreflexia after spinal cord injury in rats.

Following spinal cord transection (SCT), sensory input to the spinal cord causes increases in arterial pressure that are small in rats 1 week after SCT, but become large and well established by 2 weeks. Moreover, sympathetic preganglionic neurons (SPNs) undergo atrophy by 1 week after SCT, and regeneration of these neurons may be an important factor in the etiology of this autonomic dysreflexia. Therefore, we examined the morphology of SPNs 2 weeks after SCT using retrograde transport of the cholera toxin subunit B. The dendritic arbors of SPNs were re-established by 2 weeks after SCT. This regeneration parallels the time course of the development of autonomic dysreflexia after cord injury in the rat, and may play a role in initiating this disorder.