Functional evaluation of inhibition of autonomic transmitter release by autoantibody from Lambert-Eaton myasthenic syndrome.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 9585366.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
The effects of the anti-voltage-gated Ca2+ 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 response. 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.
Medical subject headings
- Autoantibodies
- Calcium Channels
- Lambert-Eaton Myasthenic Syndrome
- Parasympathetic Nervous System
- Receptors, Cholinergic
- omega-Conotoxins