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Immunoglobulins of Lambert‐Eaton myasthenic syndrome inhibit rat pituitary hormone release
Author(s) -
Login Ivan S.,
Kim Yong I.,
Judd Allan M.,
Spangelo Bryan L.,
MacLeod Robert M.
Publication year - 1987
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410220509
Subject(s) - lambert eaton myasthenic syndrome , endocrinology , medicine , prolactin , anterior pituitary , myasthenia gravis , calcium , chemistry , hormone , calcium channel , neuromuscular junction , antibody , activator (genetics) , incubation , biology , immunology , receptor , biochemistry , neuroscience
We speculated that IgG from patients with Lambert‐Eaton myasthenic syndrome (LES) would inhibit calciumdependent hormone secretion in rat anterior pituitary (AP) cells. Primary cultures of normal AP cells were continuously exposed to crude IgG from an LES patient or from healthy control subjects, and the incubation media were assayed for prolactin (PRL) or growth hormone (GH). The LES IgG caused a time‐ and concentration‐dependent reduction of PRL and GH release compared with control IgG over 0.5 to 48 hours using concentrations of 0.01 to 4.0 mg/ml. The calcium‐channel activator maitotoxin stimulated 45 Ca 2+ uptake and PRL release from AP cells under control conditions, and the LES IgG significantly reduced both actions of maitotoxin. Thus LES IgG appears to modulate an AP antigenic site, perhaps representing an integral component of voltage‐gated calcium channels that may share properties with similar presynaptic elements at the neuromuscular junction.