Korean J Phys Anthropol.
2004 Jun;17(2):153-161.
Abnormal Expression of Neuropeptide Y in the Cerebellar Purkinje Cells of the Ataxic Mutant Mice, Pogo
- Affiliations
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- 1Department of Anatomy & Physiology, College of Medicine, Konyang University, Nonsan, Korea. ygjeong@konyang.ac.kr
- 2Department of Pediatrics, College of Medicine, Konyang University, Nonsan, Korea.
Abstract
- The pogo mouse is an autosomal recessive ataxic mutant that arose spontaneously in the inbred KJR/MsKist strain derived originally from Korean wild mice. The ataxic phenotype is characterized by difficulty in maintaining posture and the consequent inability to walk straight. In our previous study about pogo mice cerebellum, we reported the Purkinje cell abnormalities and ectopic expression of tyrosine hydroxylase (TH) in Purkinje cell. In this study, we have provided an abnormal expression of NPY in ataxic mutant pogo mice for the first time. There was increased immunoreactivity for NPY in Purkinje cell of ataxic pogo (pogo/pogo) mice compared to those of heterozygote non-ataxic pogo mice (pogo/+, control group). In our previous study, TH is also expressed abnormally in Purkinje cells of ataxic mutant pogo (pogo/pogo) mouse cerebellum. To compare the expression patterns of TH and NPY within some Purkinje cell using double immunofluorescence, most of NPY-immunoreactive Purkinje cells in the ataxic pogo mice are TH-immunoreactive Purkinje cells. However, all of TH-immunoreactive Purkinje cells are not express the NPY. These data reveal that abnormal NPY-immunoreactivity in the ataxic pogo (pogo/pogo) cerebellum is restricted to a subset of cells within the ectopic TH-immunoreactive Purkinje cell subset. These results further suggest that Purkinje cell abnormalities contribute to motor ataxia in the ataxic pogo mouse.