Selective disruption of neurotransmission by acetylcholinesterase antibodies in sympathetic ganglia examined with intracellular microelectrodes

Steven M. Miller, Leonid G. Ermilov, Joseph H. Szurszewski, Pamela I. Hammond, Stephen Brimijoin

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Antibodies to acetylcholinesterase (AChE) induce adrenergic dysfunction in rats by selective, complement-mediated destruction of preganglionic sympathetic nerve terminals. To analyze this phenomenon at the neuronal level, monoclonal antibodies to AChE (1.6 mg) were injected via the tail vein, and superior cervical ganglia (SCG) or inferior mesenteric ganglia (IMG) were studied in vitro. In control SCG, all impaled neurons generated action potentials during direct injection of depolarizing current or indirect stimulation through the preganglionic nerve. Current 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 transmission was much less affected by antibody exposure: 60% or more of examined neurons responded to preganglionic stimulation. Differences in antibody access did not explain differing sensitivities of SCG and IMG since immunohistochemistry showed rapid accumulation of IgG deposits in both ganglia. These results are believed to reflect widespread but subtotal preganglionic sympathectomy by AChE antibodies. Current information indicates that paravertebral ganglia are all antibody-sensitive, but some pre vertebral ganglia are resistant, suggesting immunochemical differences between them.

Original languageEnglish (US)
Pages (from-to)156-167
Number of pages12
JournalJournal of the autonomic nervous system
Volume67
Issue number3
DOIs
StatePublished - Dec 11 1997

    Fingerprint

Keywords

  • Adrenergic dysfunction
  • Blood-ganglion barrier
  • Colonofugal nerves
  • Complement-mediated neural lesion
  • Dysautonomia
  • Inferior mesenteric ganglion
  • Preganglionic neurons
  • Superior cervical ganglion
  • Sypnaptophysin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Clinical Neurology

Cite this