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

Citation
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
Citations number
31
Categorie Soggetti
Neurosciences,"Clinical Neurology
ISSN journal
10859489
Volume
3
Issue
2
Year of publication
1998
Pages
103 - 109
Database
ISI
SICI code
1085-9489(1998)3:2<103:PCONIM>2.0.ZU;2-I
Abstract
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.