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作 者:刘睿[1] 李柱一[1] 吴玉梅[2] 许汉鹏[2] 王者晋[1]
机构地区:[1]第四军医大学唐都医院神经内科,陕西西安710038 [2]第四军医大学神经科学研究所,陕西西安710032
出 处:《中风与神经疾病杂志》2005年第1期13-15,共3页Journal of Apoplexy and Nervous Diseases
基 金:国家自然科学基金资助项目 (3 9970 2 67)
摘 要:目的 本研究从离体细胞水平探讨重症肌无力 (MG)患者 CNS受损的可能机制。方法 从 MG患者和正常人血中提取 Ig G。体外培养新生 SD大鼠皮层神经元 ,用免疫组化法观察 ACh RAb与神经元 n ACh R免疫结合反应 ,并行神经元胞浆钙测定。结果 MG患者 Ig G可与离体培养的皮层神经元免疫结合并引起异常胞浆钙变化 ,而正常人血中提取的 Ig G则否。结论 MG患者外周 Ig G(ACh RAb)可与离体培养的神经元 n ACh R结合并引起神经元生理活性变化 ,是 MG患者 CNS受损的可能机制。Objective To reveal the mechanism of CNS involvement with MG on cell level in vitro. Methods The primary cultured neurons were dissociated from cerebral cortex of newborn rats. Immunoreactions between AChRAb and neuronal AChR on neurons were investigated by using immuhistochemical method,the intracellular Ca[2+] ion was measured at the same time. Results The positive immunoreactions and abnormal reactions of calcium ion were found on those used IgG purified from MG patients sera,the negative reactions were found by using IgG from healthy control. Conclusion It is concluded that AChRAb of MG patients may bind to neuronal nAChR on cultured neurons and induce their physiological changes,that may cause CNS dysfuntion in MG.
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