Reflex and Morphological Changes in Spinal Preganglionic Neurons After Cord Injury in Rats

Abstract

Autonomic dysreflexia manifested as episodic hypertension after spinal cord injury may occur because of changes in sympathetic preganglionic neurons (SPNs) in response to loss of bulbospinal inputs. We studied dysreflexia in rats one week after midthoracic spinal cord hemisection or complete transection. After cord hemisection at the fifth thoracic segment all rats had hemiparaplegia and after complete transection they were paraplegic and exhibited dysreflexia characterized by pressor responses to distension of the urinary bladder. Changes in morphology of SPNs retrogradely labelled by cholera toxin and Fluoro Gold were examined and changes also were assessed in expression of the synaptic vesicular protein synaptophysin. A comparison of SPNs rostral and caudal to the lesion revealed significant dendritic degeneration and decreased soma size after the loss of supraspinal input. Expression of synaptophysin was normally observed rostral to a cord hemisection but this immunoreactivity was increased caudal to the lesion. In conclusion significant structural changes in SPNs occur within a week after cord injury. The abnormal cardiovascular control and exaggerated reflex reactions may be due to new synapse formation on these SPNs.

Key Words:

• autonomic dysreflexia
• arterial blood pressure
• synaptophysin
• preganglionic degeneration