Kim Y I
Muscle Nerve. 1985 Feb;8(2):162-72. doi: 10.1002/mus.880080213.
Mice were given 1 to 67 daily injections of whole plasma from a control subject and a patient with the Lambert-Eaton myasthenic syndrome (LES), and the parameters of neuromuscular transmission in diaphragm muscles were studied in vitro. In animals that received 41 to 59 injections of LES plasma, mean quantum content of the endplate potentials, as measured under the conditions of low [Ca2+]o (1.2 mM) and high [Mg2+]o (10 mM), was reduced to 30% of the control, or 40% of the value found in normal untreated mice. When [K+]o was elevated from 5 mM to 17.5 mM, the frequency of spontaneous miniature endplate potentials increased by a factor of 98 and 105 respectively in the control and normal mice but only 39 times in the LES plasma recipients. Despite these presynaptic abnormalities, no evidence of postsynaptic deficit, nerve conduction failure, or inability of the muscle fibers to produce normal action potentials was found. These electrophysiologic features in mice thus represent a reproduction of the human condition, supporting the concept of humoral involvement in the pathophysiology of LES. Passively transferred LES in mice is a faithful animal model of the human disease which will be useful in exploring the molecular basis of the presynaptic impairment.
给小鼠每日注射1至67次来自一名对照受试者和一名患有兰伯特-伊顿肌无力综合征(LES)患者的全血浆,然后在体外研究膈肌神经肌肉传递的参数。在接受41至59次LES血浆注射的动物中,在低[Ca2+]o(1.2 mM)和高[Mg2+]o(10 mM)条件下测量的终板电位平均量子含量降至对照值的30%,或正常未处理小鼠中发现值的40%。当[K+]o从5 mM升高到17.5 mM时,对照小鼠和正常小鼠中自发微小终板电位的频率分别增加了98倍和105倍,但接受LES血浆的小鼠中仅增加了39倍。尽管存在这些突触前异常,但未发现突触后缺陷、神经传导衰竭或肌肉纤维无法产生正常动作电位的证据。因此,小鼠中的这些电生理特征代表了人类疾病状态的重现,支持体液参与LES病理生理学的概念。小鼠中被动转移的LES是人类疾病的可靠动物模型,将有助于探索突触前损伤的分子基础。