FUNCTIONAL-EVALUATION OF INHIBITION OF AUTONOMIC TRANSMITTER RELEASE BY AUTOANTIBODY FROM LAMBERT-EATON MYASTHENIC SYNDROME

The effects of the anti-voltage-gated Ca2+ channel (VGCC) antibody obt ained from patients with Lambert-Eaton myasthenic syndrome (LEMS) on a utonomic neurotransmission were studied in in-vitro experiments. The r eleases of acetylcholine (ACh) and norepinephrine from the autonomic n erves were evaluated by changes in the contractile responses of guinea pig taenia caeci and left atria to electric field stimulation, respec tively. Incubations for 6 hours with LEMS serum and IgG, both of which contain anti-VGCC antibody, markedly suppressed the parasympathetic r esponse but did not affect the sympathetic response. Pharmacological e xperiments with specific blockers to the VGCC subtypes showed that the Q-type VGCC is closely linked to the genesis of the parasympathetic r esponse. We suggest that the anti-VGCC antibody from the LEMS patients specifically reduces the ACh release from the parasympathetic nerve b y binding to the Q-type VGCC.