alexa Is Anti-Gliadin Antibody Pathogenic in Gluten Ataxia? Analysis using Rat Cerebellar Slices and Patch-Clamp Recording
ISSN: 2168-975X

Brain Disorders & Therapy
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Research Article

Is Anti-Gliadin Antibody Pathogenic in Gluten Ataxia? Analysis using Rat Cerebellar Slices and Patch-Clamp Recording

Hiroshi Mitoma1*, Kazunori Nanri2 and Hidehiro Mizusawa3
1Department of Medical Education, Tokyo Medical University, Tokyo, Japan
2Department of Neurology, Tokyo Medical University Hachioji Medical Center, Tokyo, Japan
3Department of Neurology and Neurological Science, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
Corresponding Author : Hiroshi Mitoma
Department of Medical Education
Tokyo Medical University, Tokyo, Japan
E-mail: [email protected]
Received May 22, 2013; Accepted September 04, 2013; Published September 06, 2013
Citation: Mitoma H, Nanri K, Mizusawa H (2013) Is Anti-Gliadin Antibody Pathogenic in Gluten Ataxia? Analysis using Rat Cerebellar Slices and Patch-Clamp Recording. Brain Disord Ther 2:105. doi:10.4172/2168-975X.1000105
Copyright: © 2013 Mitoma H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The significance of autoantibodies associated withneurologicalsymptoms has been the focus of interest. Recentstudies emphasized the pathogenic role of anti-gliadin antibody in gluten ataxia, an important disease of autoimmune cerebellar ataxia. To examine whether autoantibodies, including anti-gliadin antibody, play a pathogenic role, we analyzed the effects of CSF samples obtained from a Japanese patient with gluten ataxia on cerebellar synaptic transmission. Patch-clamp recordings were prepared from cerebellar Purkinje cells, the output cells from the cerebellar cortex, in mice cerebellar slices. The CSF (diluted 1:100) had no effects on the excitatory postsynaptic currents, and did not affect the release mechanisms of glutamate. These results do not support an idea that CSF autoantibodies, including anti-gliadin antibody, interfere cerebellar synaptic function so as to develop ataxia

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