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TheScientificWorldJOURNAL
Volume 10 (2010), Pages 2032-2038
http://dx.doi.org/10.1100/tsw.2010.205
Mini-Review Article

Zebrin II Expressing Purkinje Cell Phenotype—Related and—Unrelated Cerebellar Abnormalities in Ca˅2.1 Mutant, Rolling Mouse Nagoya

1Laboratory of Anatomy, Department of Physical Therapy, Faculty of Medical and Health Sciences, Tsukuba International University, Tsuchiura, Ibaraki, Japan
2Department of Anatomy and Developmental Neurobiology, University of Tokushima Graduate School, Institute of Health Biosciences, Tokushima, Japan

Received 24 December 2009; Revised 4 October 2010; Accepted 5 October 2010

Academic Editor: Sergi Ferre

Copyright © 2010 Kazuhiko Sawada and Yoshihiro Fukui.

Abstract

Rolling mouse Nagoya is an ataxic mutant mouse that carries a mutation in a gene encoding for the alpha 1A subunit of the voltage-gated P/Q-type Ca2+ channel (Ca˅2.1). This report summarizes our studies and others concerning cerebellar abnormalities in rolling mice based on chemical neuroanatomy. While there are no obvious cerebellar deformations in this mutant mouse, the altered functions of Purkinje cells can be revealed as a reduced expression of type 1 ryanodine receptor (RyR1) in all Purkinje cells uniformly throughout the cerebellum, and as an ectopic expression of tyrosine hydroxylase (TH) in the Purkinje cell subsets with the zebrin II—immunopositive phenotype. As the mutated Ca˅2.1 channel is expressed at uniform levels in all Purkinje cells, its copresence with RyR1 staining suggests that a Ca˅2.1 channel dysfunction links with the expression of RyR1 in Purkinje cells of rolling mice. However, an ectopic expression of TH in the Purkinje cells is topologically related to the projection of corticotrophin-releasing factor—immunopositive climbing fibers rather than expression of the mutated Ca˅2.1 channel. On the other hand, increased levels of serotonin (5-HT) in 5-HTergic fibers were revealed immunohistochemically in Purkinje cells of the vermis of rolling cerebellum. Thus, to determine whether or not cerebellar abnormalities are related to Purkinje cell populations revealed by zebrin II expression is essential for enhancing our understanding of the pathogenesis of hereditary cerebellar ataxic mutants such as rolling mice.