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  • Title: Morphological changes in sympathetic preganglionic neurons after spinal cord injury in rats.
    Author: Krassioukov AV, Weaver LC.
    Journal: Neuroscience; 1996 Jan; 70(1):211-25. PubMed ID: 8848126.
    Abstract:
    Spinal cord injury results in abnormal sympathetic control of the cardiovascular system, perhaps because of reactions of sympathetic preganglionic neurons to loss of their supraspinal afferent inputs. We investigated morphological changes in sympathetic preganglionic neurons in rats one week after midthoracic spinal cord hemisection or complete transection and one month after complete transection. Morphological changes in adrenal sympathetic preganglionic neurons retrogradely-labelled by cholera toxin were examined as well as changes in other thoracic preganglionic neurons identified by their expression of reduced nicotinamide adenine dinucleotide phosphate-diaphorase. Reactive astrogliosis around these neurons was determined by assessing changes in immunoreactivity to glial fibrillary acidic protein. Changes in immunoreactivity to the synaptic vesicular protein synaptophysin were also evaluated in these areas. One week after transection, a comparison of sympathetic preganglionic neurons rostral and caudal to the lesion revealed significant loss of dendrites and decreased cell size caudal to the injury. Reactive astrocytes surrounded sympathetic preganglionic neurons as far as six segments below the transection. Constitutive expression of synaptophysin was observed rostral to the cord hemisection and synaptophysin expression was increased caudal to the lesion by seven days after the injury. One month after transection, the dendritic arbor of preganglionic neurons was re-established and the intensity of the reactive gliosis around the preganglionic neurons was diminished throughout the thoracic cord. These findings demonstrate that sympathetic preganglionic neurons undergo significant atrophy within a week after deafferentation 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 synaptophysin in the gray matter caudal to a cord injury is consistent with fibre 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.
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