White S R, Bowker R M
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman 99164.
J Neuroimmunol. 1988 Apr;18(1):75-86. doi: 10.1016/0165-5728(88)90136-1.
Bulbospinal monoamine-containing axons appear to be severely damaged in rats with the inflammatory and demyelinating disease, experimental allergic encephalomyelitis (EAE). This paper reports that although bulbospinal serotonin axons are damaged in the disease, cell bodies of origin in the medulla oblongata retain normal morphology. However, these serotonin cells are not able to retrogradely transport the enzyme horseradish peroxidase (HRP) from terminals in the lumbar spinal cord. Most non-serotonin-containing cells in the medulla which project to the lumbar spinal cord retain the ability to retrogradely transport HRP from the lumbar cord during the disease. These findings suggest that there is some specificity to spinal cord axonal damage during EAE.
在患有炎症性脱髓鞘疾病——实验性变态反应性脑脊髓炎（EAE）的大鼠中，含延髓脊髓单胺的轴突似乎受到了严重损伤。本文报告称，尽管在该疾病中延髓脊髓5-羟色胺能轴突受损，但延髓中的起源细胞体保持正常形态。然而，这些5-羟色胺能细胞无法从腰脊髓的终末逆行转运辣根过氧化物酶（HRP）。在疾病期间，延髓中大多数投射至腰脊髓的非5-羟色胺能细胞仍保留从腰脊髓逆行转运HRP的能力。这些发现表明，EAE期间脊髓轴突损伤存在一定的特异性。
