RT Journal Article
SR Electronic
T1 Presynaptic inhibition of cerebellar GABAergic transmission by glutamate decarboxylase autoantibodies in progressive cerebellar ataxia
JF Journal of Neurology, Neurosurgery & Psychiatry
JO J Neurol Neurosurg Psychiatry
FD BMJ Publishing Group Ltd
SP 386
OP 389
DO 10.1136/jnnp.70.3.386
VO 70
IS 3
A1 H Takenoshita
A1 M Shizuka-Ikeda
A1 H Mitoma
A1 S-Y Song
A1 Y Harigaya
A1 Y Igeta
A1 M Yaguchi
A1 K Ishida
A1 M Shoji
A1 M Tanaka
A1 H Mizusawa
A1 K Okamoto
YR 2001
UL http://jnnp.bmj.com/content/70/3/386.abstract
AB Autoantibodies against glutamic acid decarboxylase (GAD) have been found in stiff-man syndrome, insulin dependent diabetes mellitus, and progressive cerebellar ataxia. A patient with progressive cerebellar ataxia is described who was positive for GAD autoantibodies, and had Sjögren's syndrome. Immunohistochemical studies using CSF and serum samples from the patient showed immunoreactivities in axon terminals of cerebellar GABAergic neurons. A whole cell patch clamp technique recording from rat cerebellar slices showed that the CSF, presumably through GAD autoantibodies, presynaptically inhibited GABAergic transmission. Intravenous administration of immunoglobulin failed to improve clinical symptoms and immunoreactivities examined after therapy. The findings suggest that GAD autoantibodies play a pathogenic part in reducing GABA release in in vitro slices.