Schmidt R E, McAtee S J, Plurad D A, Parvin C A, Cogswell B E, Roth K A
Department of Pathology, Washington University School of Medicine, Saint Louis, MO 63110.
Brain Res. 1988 Sep 20;460(2):214-26. doi: 10.1016/0006-8993(88)90366-6.
To investigate the response of selected sympathetic ganglia to experimental injury, neonatal rat pups were treated with either 6-hydroxydopamine (6-OHDA), guanethidine, or antiserum to nerve growth factor (anti-NGF). When examined at one month of age, each of the treatments resulted in a significantly greater loss of neurons and tyrosine hydroxylase activity in paravertebral (superior cervical and stellate) versus prevertebral (superior mesenteric and celiac) sympathetic ganglia. Guanethidine treatment produced the largest differential in neuron loss and tyrosine hydroxylase activity between pre- and paravertebral ganglia. Histologically, the acute phase of guanethidine-induced injury in the superior cervical, paravertebral, ganglia was characterized by a prominent mononuclear cell infiltrate and extensive neuronal degeneration. Minimal histopathologic changes were seen in the superior mesenteric, prevertebral, ganglia of the same animals. Immunolocalization of tyrosine hydroxylase and neuropeptide Y (NPY) in guanethidine-treated animals showed a preferential loss of sympathetic innervation of the extramural mesenteric vasculature with relative sparing of the noradrenergic innervation of Auerbach's myenteric plexus. Differences in the susceptibility of sympathetic ganglia to various insults may underlie the selective and heterogeneous involvement of sympathetic ganglia in clinical and experimental situations.
为了研究特定交感神经节对实验性损伤的反应,对新生大鼠幼崽分别用6-羟基多巴胺(6-OHDA)、胍乙啶或抗神经生长因子抗血清(抗-NGF)进行处理。在1月龄时进行检查,结果发现,与椎前(肠系膜上和腹腔)交感神经节相比,每种处理均导致椎旁(颈上和星状)交感神经节中神经元和酪氨酸羟化酶活性显著丧失更多。胍乙啶处理在椎前和椎旁神经节的神经元丧失和酪氨酸羟化酶活性方面产生的差异最大。组织学上,胍乙啶诱导的颈上椎旁神经节损伤急性期的特征是显著的单核细胞浸润和广泛的神经元变性。在同一动物的肠系膜上椎前神经节中可见最小的组织病理学变化。胍乙啶处理动物中酪氨酸羟化酶和神经肽Y(NPY)的免疫定位显示,肠系膜外血管的交感神经支配优先丧失,而奥尔巴赫肌间神经丛的去甲肾上腺素能神经支配相对保留。交感神经节对各种损伤的易感性差异可能是交感神经节在临床和实验情况下出现选择性和异质性受累的基础。