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Selective suppression of cerebellar GABAergic transmission by an autoantibody to glutamic acid decarboxylase
Author(s) -
Ishida Kazuyuki,
Mitoma Hiroshi,
Song SiYoung,
Uchihara Toshiki,
Inaba Akira,
Eguchi Satoru,
Kobayashi Takayoshi,
Mizusawa Hidehiro
Publication year - 1999
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/1531-8249(199908)46:2<263::aid-ana19>3.0.co;2-0
Subject(s) - glutamate decarboxylase , cerebellar ataxia , autoantibody , gabaergic , ataxia , cerebellum , neuroscience , neurotransmission , cerebrospinal fluid , chemistry , medicine , biology , antibody , immunology , biochemistry , receptor , enzyme , inhibitory postsynaptic potential
Humoral immune response to glutamic acid decarboxylase (GAD) has been implicated in the pathogenesis of stiff‐man syndrome and cerebellar ataxia, but the underlying pathomechanism is unclear. Using a whole‐cell patch‐clamp technique with rat cerebellar slices, we found that immunoglobulins present in the cerebrospinal fluid of an ataxic patient acted presynaptically to cause a selective suppression of GABAergic transmission. This synaptic depression was most likely elicited by an autoantibody to GAD. Ann Neurol 1999;46:263–267