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Heat shock proteins (Hsps) are generally known to be induced in response to a range of stressfulstimuli such as hyperthermia, immobilization, UV radiation, arsenite, various chemicals, and drugs. In addition, theseproteins have been suggested to have roles in protecting cells against apoptotic cell death. The ataxic mutant Pogo(pogo/pogo) mouse is a novel neurological ataxic mutant, which is derived from Korean wild type mouse (KJR/Mskist)strain. Pogo mutation is considered as an alleles of α subunit of P/Q-type calcium channel mutants such as rollingmouse Nagoya (RMN), tottering, and leaner. We investigated the topographical Hsp25 expression using immunohistochemistryand western blot analysis in several ataxic mutant mice: RMN, tottering, leaner, Pogo and Korean wildmouse. In the cerebellum of the RMN, tottering, leaner, and normal mouse including Balb/C, C57BL/ 6 and ICR mouse,Hsp25 was expressed in a subset of Purkinje cells that form parasagittal stripes. The Hsp25 expression is largely restrictedto specific cerebellar lobules: VI /VII (the central zone: CZ), and IX/X (the nodular zone: NZ). Surprisingly, noHsp25-immunoreactive Purkinje cells were seen in CZ and NZ of the cerebellum of Pogo (pogo/pogo), heterozygotesPogo (pogo/+), and Korean wild mouse. Moreover, in western blot analysis, there was no cerebellar Hsp25 expressionin ataxic Pogo mouse including Korean wild mouse. These data suggest that cerebellar Hsp25 expression was irrelevantwith the development of ataxia in Pogo mouse.