Le W D, Engelhardt J, Xie W J, Schneider L, Smith R G, Appel S H
Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA.
J Neuroimmunol. 1995 Mar;57(1-2):45-53. doi: 10.1016/0165-5728(94)00160-p.
An animal model of experimental autoimmune nigral damage (EAND) has been developed in guinea pigs by immunization with hybrid dopaminergic cells (MES 23.5). In such animals, loss of 40% of the substantia nigra (SN) neurons and damage to an additional 10% of SN neurons was associated with a 37-43% decrease of tyrosine hydroxylase (TH) activity and a 36% decrease of dopamine (DA) content in the nigral-striatum. Eight of the thirteen animals developed significant hypokinesia. The EAND model suggests that degeneration of dopaminergic neurons in SN can be caused by immune-mediated processes, which may help our understanding of the pathogenesis in Parkinson's disease.
通过用杂交多巴胺能细胞（MES 23.5）免疫豚鼠，建立了实验性自身免疫性黑质损伤（EAND）的动物模型。在这类动物中，黑质（SN）40%的神经元丧失，另外10%的SN神经元受损，同时黑质纹状体中酪氨酸羟化酶（TH）活性降低37%-43%，多巴胺（DA）含量降低36%。13只动物中有8只出现明显的运动功能减退。EAND模型表明，SN中多巴胺能神经元的变性可能由免疫介导的过程引起，这可能有助于我们理解帕金森病的发病机制。
