The myasthenic (Eaton-Lambert) syndrome associated with carcinoma. Enzyme induction as a possible mechanism of paraneoplastic syndromes.
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.
D000109:Acetylcholine / Q000378:metabolism; D000110:Acetylcholinesterase / Q000378:metabolism; D001327:Autoimmune Diseases / Q000150:complications; D018288:Carcinoma, Small Cell / Q000150:complications* / Q000201:enzymology; D004790:Enzyme Induction; D006801:Humans; D008175:Lung Neoplasms / Q000150:complications* / Q000201:enzymology; D009157:Myasthenia Gravis / Q000150:complications* / Q000201:enzymology; D010257:Paraneoplastic Syndromes / Q000201:enzymology*
D000110:Acetylcholinesterase; D000109:Acetylcholine