Pflügers Archiv

, Volume 390, Issue 2, pp 156–160 | Cite as

Neuromuscular transmission in experimental autoimmune myasthenia gravis (EAMG)

Quantitative ionophoresis and current fluctuation analysis at normal and myasthenic rat end-plates
  • Reinhard Hohlfeld
  • Raimund Sterz
  • Inge Kalies
  • Klaus Peper
  • Hartmut Wekerle
Excitable Tissues and Central Nervous Physiology


Chronic experimental autoimmune myasthenia gravis (EAMG) was induced in rats by immunization with acetylcholine receptor (AChR) purified from the electroplax of Torpedo californica. 35–40 days after immunization, serum anti-AChR antibody titers were about 40 nM. At this stage, electrophysiology was performed on isolated M. omohyoideus muscle-preparations from myasthenic and from normal (control) rats.

For the study of the equilibrium interaction between acetylcholine (ACh) and AChR, dose-response curves were obtained by quantitative ionophoretic application of ACh to voltage-clamped end-plates. Analysis of dose-response curves yielded the following parameters: maximum end-plate conductance per unit surfacegmax (EAMG)=10.3±1.1 nS/μm2,gmax (normal)=20.2±1.8 nS/μm2; apparent dissociation constant K (EAMG)=96±5 μM, K (normal)=58±6 μM; Hill-coefficient nH (EAMG)=2.3±0.1, nH (normal)=2.3±0.1. Single channel properties were derived from an analysis of ACh-induced end-plate current noise: the mean single channel conductance was γ(EAMG)=29.1±2.2 pS, γ(normal)=27.6±1.8 pS and the mean channel life-time τ(EAMG)=1.39±0.09 ms, τ(normal)=1.32±0.08 ms (T=22°C).

The electrophysiological data are interpreted as follows: (1) At myasthenic end-plates there is a 50–60% reduction of functioning AChR (decrease ofgmax). A total number of about 2×106 (1×106) channels per end-plate was calculated for control (myasthenic) rats. (2) The affinity of AChR for ACh is reduced and/or there is an impediment of the conformational change from the closed- to the open-channel configuration (increase of K). (3) Single channel properties are essentially unaffected.

Key words

Myasthenia gravis Experimental autoimmune myasthenia gravis Acetylcholine receptor Quantitative ionophoresis Neuromuscular junction 


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Copyright information

© Springer-Verlag 1981

Authors and Affiliations

  • Reinhard Hohlfeld
    • 1
  • Raimund Sterz
    • 2
  • Inge Kalies
    • 3
  • Klaus Peper
    • 2
  • Hartmut Wekerle
    • 1
  1. 1.Max-Planck-Institut für ImmunbiologieFreiburg
  2. 2.II. Physiologisches InstitutHomburg/Saar
  3. 3.Zentrum BiochemieHannoverFederal Republic of Germany

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