IgM monoclonal antibody against terminal moiety of GM2, GalNAc-GD1a and GalNAc-GM1b from a pure motor chronic demyelinating polyneuropathy patient:: effects on neurotransmitter release

被引:38
作者
Ortiz, N
Rosa, R
Gallardo, E
Illa, I
Tomas, J
Aubry, J
Santafé, M
机构
[1] Univ Rovira & Virgili, Fac Med & Hlth Sci, Histol & Neurobiol Unit, E-43201 Reus, Spain
[2] St Joan Univ Hosp, Dept Med, Neurol Sect, Reus 43201, Spain
[3] Univ Rovira & Virgili, Fac Med & Hlth Sci, Dept Med & Surg, E-43201 Reus, Spain
[4] St Pau Hosp, Dept Neurol, Barcelona 08025, Spain
[5] Univ Nantes, F-44035 Nantes 01, France
[6] Inst Biol, INSERM, U463, F-44035 Nantes 01, France
关键词
monoclonal IgM component; neurotransmitter release; motor chronic demyelinating polyneuropathy;
D O I
10.1016/S0165-5728(01)00373-3
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We describe a patient with a pure motor chronic demyelinating polyneuropathy with an IgM monoclonal component showing anti-GM2, GalNAc-GD1a and GalNAc-GM1b reactivity whose common epitope appears to be -[GalNAc beta1-4Gal(3-2 alpha NeuAc)beta1]. We used intracellular recording to study how IgM from this patient affected neurotransmitter release in the mouse diaphragm in vitro. Adding serum (and specifically, the purified monoclonal IgM component) blocked the nerve-evoked response in both quantal content and evoked endplate potential (EPP) amplitude in a complement-independent and reversible manner. The IgM increased the frequency of spontaneous miniature endplate potentials (MEPPs) in a complement-dependent and reversible manner but had no effect on MEPP amplitude. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:114 / 123
页数:10
相关论文
共 40 条
[1]   Gangliosides and sialylcholesterol as modulators of synaptic functions [J].
Ando, S ;
Tanaka, Y ;
Waki, H ;
Kon, K ;
Iwamoto, M ;
Fukui, F .
SPHINGOLIPIDS AS SIGNALING MODULATORS IN THE NERVOUS SYSTEM, 1998, 845 :232-239
[2]   IMMUNOGLOBULINS FROM ANIMAL-MODELS OF MOTOR-NEURON DISEASE AND FROM HUMAN AMYOTROPHIC-LATERAL-SCLEROSIS PATIENTS PASSIVELY TRANSFER PHYSIOLOGICAL ABNORMALITIES TO THE NEUROMUSCULAR-JUNCTION [J].
APPEL, SH ;
ENGELHARDT, JI ;
GARCIA, J ;
STEFANI, E .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (02) :647-651
[3]   ACUTE CONDUCTION BLOCK INVITRO FOLLOWING EXPOSURE TO ANTIGANGLIOSIDE SERA [J].
ARASAKI, K ;
KUSUNOKI, S ;
KUDO, N ;
KANAZAWA, I .
MUSCLE & NERVE, 1993, 16 (06) :587-593
[4]   Antiglycolipid antibodies in motor neuropathies [J].
Baumann, N ;
Harpin, ML ;
Marie, Y ;
Lemerle, K ;
Chassande, B ;
Bouche, P ;
Meininger, V ;
Yu, RK ;
Léger, JM .
SPHINGOLIPIDS AS SIGNALING MODULATORS IN THE NERVOUS SYSTEM, 1998, 845 :322-329
[5]   Neuromuscular blockade by IgG antibodies from patients with Guillain-Barre syndrome: A macro-patch-clamp study [J].
Buchwald, B ;
Toyka, KV ;
Zielasek, J ;
Weishaupt, A ;
Schweiger, S ;
Dudel, J .
ANNALS OF NEUROLOGY, 1998, 44 (06) :913-922
[6]  
Bullens RWM, 2000, MUSCLE NERVE, V23, P1035, DOI 10.1002/1097-4598(200007)23:7<1035::AID-MUS5>3.3.CO
[7]  
2-I
[8]  
CARLSON RO, 1994, J NEUROSCI, V14, P2272
[9]   SERUM IGG ANTIBODY TO GANGLIOSIDE GQ1B IS A POSSIBLE MARKER OF MILLER FISHER SYNDROME [J].
CHIBA, A ;
KUSUNOKI, S ;
SHIMIZU, T ;
KANAZAWA, I .
ANNALS OF NEUROLOGY, 1992, 31 (06) :677-679
[10]   SENSORY NEUROPATHY ASSOCIATED WITH MONOCLONAL IMMUNOGLOBULIN-M TO GD1B GANGLIOSIDE [J].
DAUNE, GC ;
FARRER, RG ;
DALAKAS, MC ;
QUARLES, RH .
ANNALS OF NEUROLOGY, 1992, 31 (06) :683-685