Systemic injection of monoclonal antibodies to neural acetylcholinesterase in adult rats caused a syndrome with permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensued. In sympathetic ganglia, acetylcholinesterase activity disappeared from neuropil but not from nerve cell bodies. Choline acetyltransferase activity and ultrastructurally defined synapses were also lost. Electrical stimulation of presynaptic fibers to the superior cervical ganglion ceased to evoke end-organ responses.
This model of selective cholinergic autoimmunity represents another tool for autonomic physiology and may be r
elevant to the pathogenesis of human dysautonomias.
S Brimijoin and V A Lennon
Department of Pharmacology, Mayo Clinic, Rochester, MN 55905.
Proc Natl Acad Sci U S A. 1990 December; 87(24): 9630–9634.