Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Cells, Cultured
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Embryo, Mammalian
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Female
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GABAergic Neurons / cytology*
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GABAergic Neurons / drug effects
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Glutamate Decarboxylase / immunology*
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Hippocampus / cytology
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Humans
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Immunoglobulin G / pharmacology*
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In Vitro Techniques
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Inhibitory Postsynaptic Potentials / drug effects*
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Inhibitory Postsynaptic Potentials / physiology
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Male
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Mice
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Mice, Inbred C57BL
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Microscopy, Confocal
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Neurotransmitter Agents / pharmacology
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Patch-Clamp Techniques
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Presynaptic Terminals / drug effects*
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Presynaptic Terminals / metabolism
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Statistics, Nonparametric
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Stiff-Person Syndrome / immunology
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Stiff-Person Syndrome / metabolism*
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Synaptophysin / metabolism
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Vesicular Inhibitory Amino Acid Transport Proteins / metabolism
Substances
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Immunoglobulin G
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Neurotransmitter Agents
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Synaptophysin
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Vesicular Inhibitory Amino Acid Transport Proteins
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Viaat protein, mouse
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Glutamate Decarboxylase
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glutamate decarboxylase 2