Potentiation of a functional autoantibody in narcolepsy by a cholinesterase inhibitor.

摘要: We have recently reported the presence of an immunoglobulin G (IgG) autoantibody (Ab) in patients with narcolepsy cataplexy that abolishes spontaneous colonic migrating motor complexes (CMMCs) and increases smooth muscle tension atropine-sensitive phasic contractions a physiological assay isolated colon. In this study, we used cholinesterase inhibitor, neostigmine, to explore mechanism narcoleptic IgG-mediated disruption enteric function four identify pharmacological mimic Ab. Neostigmine potentiated increase resting by but exerted no effect on control IgG. Decreased frequency CMMCs mediated IgG anti-M3R activity was reversed neostigmine. Therefore, challenge inhibitor improves specificity CMMC for Tetrodotoxin (TTX), neuronal sodium channel blocker, also abolished increased tone, similar potentiation observed neostigmine; thus, TTX is functional effects bioassay. These findings provide link studies canine are consistent blockade both excitatory inhibitory neurons Ab, mimic, presumably binding autoantigenic target expressed populations neurons.