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重症肌无力患者烟碱型乙酰胆碱受体抗体致鼠脑干听觉诱发电位 被引量:33

Mechanism of the Central Involvement in EAMG:Ⅰ. Dysfunction of Rat BAEP by nAChRab of MG
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摘要 目的神经肌接头(NMJ)处乙酰胆碱(ACh)传递障碍,是重症肌无力(MG)发病机制。然而,近年有研究表明部分MG患者有中枢神经系统(CNS)受损的症状和神经电生理方面的异常表现,本研究为探讨其机制。方法从烟碱型乙酰胆碱受体抗体(nAChR-ab)阳性的全身型MG患者血清中提取IgG,将其注入SD大鼠脑室系统,观察其对脑干听觉诱发电位(BAEP)的影响。结果nAChR-ah使脑干听觉传导功能异常,表现为Ⅰ波后各波消失,Ⅰ-Ⅲ、Ⅰ-ⅤIPLs延长,Ⅴ/Ⅰ波幅比值降低。表明MG患者nAChR-ab可能与CNS中的神经-烟碱型乙酰胆碱受体(神经-nAChR)结合,BAEP异常可能与nAChR-ab结合听觉通路中继核团有关。结论nAChR-ah的病理作用不仅只限于NMJ处的nAChR,还可波及到脑干处的nAChR。 Objective Myasthenia gravis (MG) is generally accepted as an autoimmune disease inwhich circulating antibodies, acetylcholine receptor antibodies (AChRabs) against the muscle type nicotinic AChR causing a disorder of conduction at the neuromuscular junction.However, there is an increasing body of evidence of the involvement of the CNS in certainpercentage of MG. The mechanism of central involvement, however, remained unexplored.Methods In the present study brainstem auditory evoked potential (BAEP) examinationwas applied before and after injection of AChRab purified from MG sera into the rats cerebralventricular system to investigate the possibility of attack of the central nervous system by peripheral AChRab in MG. Results BAEP examination revealed that prolongation of interpeak latencies of major components Ⅰ-Ⅲ and Ⅰ- Ⅴ,decrease of Ⅴ/Ⅰratio or/and loss ofmaJor components compared to prior injections of AChRab. Conclusion It is concluded thatAChRab presented in MG sera not only bind to muscle type nicotinic AChR but may also attack of central nervous system.
出处 《中国神经免疫学和神经病学杂志》 CAS 1998年第1期1-5,共5页 Chinese Journal of Neuroimmunology and Neurology
关键词 重症肌无力 乙酰胆碱 受体 听觉诱发电位 myasthenia gravis muscular nicotinic acetylcholine receptor acetylcholine receptor antibody brain stem auditory evoked potential
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