SELECTIVE DISRUPTION OF NEUROTRANSMISSION BY ACETYLCHOLINESTERASE ANTIBODIES IN SYMPATHETIC-GANGLIA EXAMINED WITH INTRACELLULAR MICROELECTRODES

Antibodies to acetylcholinesterase (AChE) induce adrenergic dysfunctio n in rats by selective, complement-mediated destruction of preganglion ic sympathetic nerve terminals. To analyze this phenomenon at the neur onal level, monoclonal antibodies to AChE (1.6 mg) were injected via t he tail vein, and superior cervical ganglia (SCG) or inferior mesenter ic ganglia (IMG) were studied in vitro. La control SCG, all impaled ne urons generated action potentials during direct injection of depolariz ing current or indirect stimulation through the preganglionic nerve. C urrent injection remained effective in ganglia from treated rats, but preganglionic stimulation was greatly impaired: at 12 h and 3 d, less than 10% of the neurons responded, even to a maximal stimulus (150 V): at 9 d, only 25% responded. By contrast, in IMG, synaptic transmissio n was much less affected by antibody exposure: 60% or more of examined neurons responded to preganglionic stimulation. Differences in antibo dy access did not explain differing sensitivities of SCG and IMG since immunohistochemistry showed rapid accumulation of IgG deposits in bot h ganglia. These results are believed to reflect widespread but subtot al preganglionic sympathectomy by AChE antibodies. Current information indicates that paravertebral ganglia are all antibody-sensitive, but some prevertebral ganglia are resistant, suggesting immunochemical dif ferences between them. (C) 1997 Elsevier Science B.V.