Selective suppression of cerebellar GABAergic transmission by an autoantibody to glutamic acid decarboxylase.
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.
Ishida
K
K
Department of Neurology, School of Medicine, Tokyo Medical and Dental University, Japan.
Mitoma
H
H
Song
S Y
SY
Uchihara
T
T
Inaba
A
A
Eguchi
S
S
Kobayashi
T
T
Mizusawa
H
H
D000368:Aged; D001323:Autoantibodies / Q000276:immunology*; D002524:Cerebellar Ataxia / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D004594:Electrophysiology; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007150:Immunohistochemistry; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000276:immunology*
D001323:Autoantibodies; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase