Premium
Functional evaluation of inhibition of autonomic transmitter release by autoantibody from lambert eaton myasthenic syndrome
Author(s) -
Houzen Hideki,
Hattori Yuichi,
Kanno Morio,
Kikuchi Seiji,
Tashiro Kunio,
Motomura Masakatsu,
Nakao Youko,
Nakamura Tatsufumi
Publication year - 1998
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.410430520
Subject(s) - lambert eaton myasthenic syndrome , autoantibody , medicine , myasthenia gravis , neuroscience , immunology , antibody , biology
The effects of the anti–voltage‐gated Ca 2+ channel (VGCC) antibody obtained from patients with Lambert‐Eaton myasthenic syndrome (LEMS) on autonomic neurotransmission were studied in in‐vitro experiments. The releases of acetylcholine (ACh) and norepinephrine from the autonomic nerves were evaluated by changes in the contractile responses of guinea pig taenia caeci and left atria to electric field stimulation, respectively. Incubations for 6 hours with LEMS serum and IgG, both of which contain anti‐VGCC antibody, markedly suppressed the parasympathetic response but did not affect the sympathetic response. Pharmacological experiments with specific blockers to the VGCC subtypes showed that the Q‐type VGCC is closely linked to the genesis of the parasympathetic responses. We suggest that the anti‐VGCC antibody from the LEMS patients specifically reduces the ACh release from the parasympathetic nerve by binding to the Q‐type VGCC.