Stiff person-syndrome IgG affects presynaptic GABAergic release mechanisms

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 spontane...

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Bibliographic Details
Published inJournal of Neural Transmission Vol. 122; no. 3; pp. 357 - 362
Main Authors Werner, Christian, Haselmann, Holger, Weishaupt, Andreas, Toyka, Klaus V., Sommer, Claudia, Geis, Christian
Format Journal Article
LanguageEnglish
Published Vienna Springer Vienna 01.03.2015
Springer Nature B.V
Subjects
Animals
Animals, Newborn
Cells, Cultured
Embryo, Mammalian
Female
GABAergic Neurons - cytology
GABAergic Neurons - drug effects
Glutamate Decarboxylase - immunology
Hippocampus - cytology
Humans
Immunoglobulin G - pharmacology
In Vitro Techniques
Inhibitory Postsynaptic Potentials - drug effects
Inhibitory Postsynaptic Potentials - physiology
Male
Medicine
Medicine & Public Health
Mice
Mice, Inbred C57BL
Microscopy, Confocal
Neurology
Neurosciences
Neurotransmitter Agents - pharmacology
Patch-Clamp Techniques
Presynaptic Terminals - drug effects
Presynaptic Terminals - metabolism
Psychiatry
Statistics, Nonparametric
Stiff-Person Syndrome - immunology
Stiff-Person Syndrome - metabolism
Synaptophysin - metabolism
Translational Neurosciences - Short communication
Vesicular Inhibitory Amino Acid Transport Proteins - metabolism
Glutamate decarboxylase 65
GAD2
Stiff person-syndrome
Patch-clamp
Synaptic transmission
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Summary: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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SourceType-Scholarly Journals-1
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ISSN:0300-9564
1435-1463
DOI:10.1007/s00702-014-1268-1