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

Hiroshi Mitoma Kazunori Nanri

doi:10.4172/2168-975x.1000105

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

Highlights

The significance of autoantibodies associated with neurological diseases has been the focus of discussion
The present results showed that the CSF obtained from a Japanese patient with gluten ataxia did not affect excitatory cerebellar synaptic transmission
Autoimmune cerebellar ataxia is important because early diagnosis and therapy could relieve the ataxia

Summary

Introduction

The significance of autoantibodies associated with neurological diseases has been the focus of discussion. In most of autoimmune neurological disorders, it is not clear whether the antibody acts as a pathogenic agent causing symptoms, or it is produced as a result of cell-mediated autoimmune responses against neural structures. Patch-clamp recording of rat brain slices preparations for measurement of postsynaptic current is a useful method for examination of changes in signal flow in neural circuits (pathogenic action) for two reasons. Release mechanism of the transmitter, and receptor sensitivity can be detected as changes in postsynaptic current. The neural circuits are maintained in slice preparations Using this method, we reported previously that autoantibodies to GAD (GAD-Ab) played a pathogenic role in the development of neurological disorders [1,2,3]. Taken together with passive transfer experiments [4,5], GAD-Ab is established to cause cerebellar ataxia

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Discussion

Conclusion