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Acetylcholinesterase Autoimmunity In Vitro

  • H. Tang
  • P. Hammond
  • L. Ermilov
  • S. Miller
  • S. Brimijoin

Abstract

It is now established that systemic injections of antibodies to acetylcholinesterase (AChE) selectively destroy presynaptic inputs to sympathetic ganglia in rats. To investigate immunologic mechanisms, we created an in vitro model in which all components could be manipulated. Freshly dissected rat SCG were incubated 15–20 hr in Krebs solution or normal human serum (NHS) at 37 °C with continuous oxygenation. More than 96% of neurons in 6 control ganglia retained synaptic inputs as defined by action potentials or excitatory postsynaptic potentials upon stimulation of the preganglionic trunk. On the other hand, of 61 neurons from 5 ganglia incubated in NHS together with anti-AChE antibodies (0.16 mg/ml), none showed synaptic responses although membrane potential and input resistance remained normal. Antibody effects required active complement, since synaptic input was retained in 60–85% of neurons incubated with AChE antibody in NHS that was heat-inactivated (58 °C, 40 min) or immunologically depleted of C3. Likewise, choline acetyltransferase activity (marker of cholinergic cytoplasm in SCG) was largely lost after incubation with AChE antibody in NHS but was unchanged after incubation in heat-inactivated or C3-deficient NHS. These results are consistent with a disruption of AChE staining observed in SCG treated with antibody plus complement. Together, the findings clarify the role of humoral factors in immune lesions of preganglionic sympathetic terminals.

Keywords

Active Complement Synaptic Input Input Resistance Sympathetic Ganglion Immunologic Mechanism 
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Copyright information

© Springer Science+Business Media New York 1998

Authors and Affiliations

  • H. Tang
    • 1
  • P. Hammond
    • 1
  • L. Ermilov
    • 1
  • S. Miller
    • 1
  • S. Brimijoin
    • 1
  1. 1.Depts. of Pharmacology, Physiology & BiophysicsMayo ClinicRochesterUSA

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