Presynaptic impairment of cerebellar inhibitory synapses by an autoantibody to glutamate decarboxylase

H. Mitoma, S. Y. Song, K. Ishida, T. Yamakuni, T. Kobayashi, H. Mizusawa

Research output: Contribution to journalArticlepeer-review

77 Citations (Scopus)

Abstract

Glutamic acid decarboxylase (GAD), the enzyme responsible for converting glutamate to gamma-aminobutyric acid (GABA), is a target of humoral autoimmunity in stiff-man syndrome and subacute cerebellar ataxia. Recently, we found that an anti-GAD autoantibody in the CSF of an ataxic patient selectively suppressed GABA-mediated transmission on cerebellar Purkinje cells without affecting glutamate-mediated transmission. Here, we examine the mechanism by which the autoantibody impaired the inhibitory transmission, using immunohistochemistry and whole-cell recording in rat cerebellar slices. The present results indicate that CSF immunoglobulins prepared from an ataxic patient acted on the presynaptic terminals of GABAergic interneurons and decreased GABA release onto Purkinje cells. (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)40-44
Number of pages5
JournalJournal of the neurological sciences
Volume175
Issue number1
DOIs
Publication statusPublished - 2000 Apr 1

Keywords

  • Cerebellar ataxia
  • Cerebellar inhibitory synapses
  • Glutamate decarboxylase
  • Presynaptic impairment

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Fingerprint Dive into the research topics of 'Presynaptic impairment of cerebellar inhibitory synapses by an autoantibody to glutamate decarboxylase'. Together they form a unique fingerprint.

Cite this