PRESYNAPTIC CHANGES OF NEUROMUSCULAR-TRANSMISSION IN MICE INDUCED BY PASSIVE TRANSFER OF PLASMA WITH ANTI-PRESYNAPTIC MEMBRANE-RECEPTOR ANTIBODIES FROM A PATIENT WITH MYASTHENIA-GRAVIS
K. Xu et al., PRESYNAPTIC CHANGES OF NEUROMUSCULAR-TRANSMISSION IN MICE INDUCED BY PASSIVE TRANSFER OF PLASMA WITH ANTI-PRESYNAPTIC MEMBRANE-RECEPTOR ANTIBODIES FROM A PATIENT WITH MYASTHENIA-GRAVIS, Journal of the peripheral nervous system, 3(2), 1998, pp. 103-109
Electrophysiological studies were conducted in three groups of mice to
determine the possible involvement of the antibodies to presynaptic m
embrane receptor (PsmR), a beta-bungarotoxin (beta-BuTX) binding prote
in, in the pathogenesis of myasthenia gravis (MG). Mice were untreated
(untreated group, n = 8) or were injected (i.p.) with blood plasma fr
om a MG patient, which contained antibodies to PsmR: at a dose of 1 ml
per day for more than 2 months (MG plasma group, n = 12) or with plas
ma from healthy subjects (normal plasma group, n = 10). Prior to plasm
a injection, cyclophosphamide was given at 300 mg/kg (i.p.) to all thr
ee groups. About three weeks after plasma injection, most mice of the
MG plasma group became less mobile in comparison with those of the two
control groups. Electrophysiological recording showed three main chan
ges in the MG plasma group: (1) the increase in the frequency of minia
ture endplate potentials (mEPPs) induced by Krebs solution with high K
+ concentration (17.5 mM) was significantly lowered, which was confirm
ed in mice injected with IgG (50 mg per day) from this patient for two
days; (2) the quantal content of EPP was decreased; and (3) the decre
ment in the amplitude of a train EPP (50 Hz) was quickened. Our result
s suggest that this experimental model is different from that of Lambe
rt-Eaton myasthenic syndrome and that antibodies to PsmR may also be i
nvolved in the pathogenesis of MG.