MORPHOLOGICAL-CHANGES IN SYMPATHETIC PREGANGLIONIC NEURONS AFTER SPINAL-CORD INJURY IN RATS

Spinal cord injury results in abnormal sympathetic control of the card iovascular system, perhaps because of reactions of sympathetic pregang lionic neurons to loss of their supraspinal afferent inputs. We invest igated morphological changes in sympathetic preganglionic neurons in r ats one week after midthoracic spinal cord hemisection or complete tra nsection and one month after complete transection. Morphological chang es in adrenal sympathetic preganglionic neurons retrogradely-labelled by cholera toxin were examined as well as changes in other thoracic pr eganglionic neurons identified by their expression of reduced nicotina mide adenine dinucleotide phosphate-diaphorase. Reactive astrogliosis around these neurons was determined by assessing changes in immunoreac tivity to glial fibrillary acidic protein. Changes in immunoreactivity to the synaptic vesicular protein synaptophysin were also evaluated i n these areas. One week after transection, a comparison of sympathetic preganglionic neurons rostral and caudal to the lesion revealed signi ficant loss of dendrites and decreased cell size caudal to the injury. Reactive astrocytes surrounded sympathetic preganglionic neurons as f ar as six segments below the transection. Constituitive expression of synaptophysin was observed rostral to the cord hemisection and synapto physin expression was increased caudal to the lesion by seven days aft er the injury. One month after transection, the dendritic arbor of pre ganglionic neurons was re-established and the intensity of the reactiv e gliosis around the preganglionic neurons was diminished throughout t he thoracic cord. These findings demonstrate that sympathetic pregangl ionic neurons undergo significant atrophy within a week after deaffere ntation and that this reaction is reversed within one month. Reactive astrogliosis could contribute to plastic changes in the neuropil that affect the sympathetic neurons, and the enhanced expression of synapto physin in the gray matter caudal to a cord injury is consistent with f ibre outgrowth leading to new synapse formation. Such re-organization could be one of the mechanisms for disorders in blood pressure control that occur after spinal cord injury.