Simpson J A
Scott Med J. 1982 Jul;27(3):220-8. doi: 10.1177/003693308202700305.
A myasthenic syndrome associated with small-cell tumours of the bronchus and with autoimmune diseases (Eaton-Lambert syndrome) has been attributed to diminished probability that a nerve action potential will release acetylcholine (ACh) from terminals of cholinergic nerves (somatic motor and autonomic). This model derives from evidence for reduced quantal content of the transmitter released by a nerve impulse. The test procedure implies certain constancies of postsynaptic response. Abnormal responses to ACh-agonists indicate that receptor response is not normal. It is suggested that all previously described neuromuscular responses are compatible with new model: the subsynaptic apparatus produces excess acetylcholinesterase (AChE) which limits the endplate conductance changes produced by normal output of ACh. This model is supported by earlier ultramicroscopic studies which cannot be accounted for by the contemporary model. It is proposed that enzyme induction by peptide or immunoglobulin may also be responsible for other paraneoplastic syndromes.
一种与支气管小细胞肿瘤及自身免疫性疾病相关的肌无力综合征（伊顿 - 兰伯特综合征），被认为是由于神经动作电位从胆碱能神经（躯体运动和自主神经）末梢释放乙酰胆碱（ACh）的可能性降低所致。该模型源于神经冲动释放的递质量子含量减少的证据。测试程序意味着突触后反应具有一定的稳定性。对ACh激动剂的异常反应表明受体反应不正常。有人提出，所有先前描述的神经肌肉反应都与新模型相符：突触下装置产生过量的乙酰胆碱酯酶（AChE），这限制了ACh正常释放量所产生的终板电导变化。该模型得到了早期超微结构研究的支持，而当代模型无法解释这些研究结果。有人提出，肽或免疫球蛋白诱导的酶也可能是其他副肿瘤综合征的原因。
