Stiff person-syndrome IgG affects presynaptic GABAergic release mechanisms
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  • 作者:Christian Werner (1) (3)
    Holger Haselmann (1) (2)
    Andreas Weishaupt (3)
    Klaus V. Toyka (3)
    Claudia Sommer (3)
    Christian Geis (1) (2) (3)

    1. Hans-Berger Department of Neurology
    ; Jena University Hospital ; Erlanger Allee ; 07747 ; Jena ; Germany
    3. Department of Neurology
    ; University Hospital W眉rzburg ; Josef-Schneider Str. 11 ; 97080 ; W眉rzburg ; Germany
    2. Center for Sepsis Control and Care (CSCC)
    ; Jena University Hospital ; Erlanger Allee 101 ; 07747 ; Jena ; Germany
  • 关键词:Stiff person ; syndrome ; Glutamate decarboxylase 65 ; GAD2 ; Patch ; clamp ; Synaptic transmission
  • 刊名:Journal of Neural Transmission
  • 出版年:2015
  • 出版时间:March 2015
  • 年:2015
  • 卷:122
  • 期:3
  • 页码:357-362
  • 全文大小:717 KB
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  • 刊物类别:Medicine
  • 刊物主题:Medicine & Public Health
    Neurology
    Pharmacology and Toxicology
    Psychiatry
  • 出版者:Springer Wien
  • ISSN:1435-1463
文摘
The majority of patients with stiff person-syndrome (SPS) are characterized by autoantibodies to glutamate decarboxylase 65 (GAD65). In previous passive-transfer studies, SPS immunoglobulin G (IgG) induced SPS core symptoms. We here provide evidence that SPS-IgG causes a higher frequency of spontaneous vesicle fusions. Sustained GABAergic transmission and presynaptic GABAergic vesicle pool size remained unchanged. Since these findings cannot be attributed to anti-GAD65 autoantibodies alone, we propose that additional autoantibodies with so far undefined antigen specificity might affect presynaptic release mechanisms.

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