1Laboratory of Anatomy Department of Physical Therapy, Faculty of Medical and Health Sciences, Tsukuba International University, Tsuchiura, Ibaraki, 300–0051, Japan
2Department of Anatomy and Developmental Neurobiology, University of Tokushima Graduate School Institute of Health Biosciences, Tokushima, 700–8503, Japan
*Correspondence: Kazuhiko Sawada, Phone: +81-29-883-6032 FAX: +81-29-826-6776, E-mail: k-sawada@tius-hs.jp
The present study quantitatively examined torpedoes of the Purkinje cell axons in deep ce-rebellar nuclei of rolling mouse Nagoya. Calbindin D-28 k immunostaining revealed a number of torpedoes throughout all three subdivisions of deep cerebellar nuclei in rolling mice, but very few in control mice. Some torpedoes were closely apposed to large- or medium-sized neurons in deep cerebellar nuclei. Torpedoes in all three subdivisions of deep cerebel-lar nuclei were significantly denser in rolling mice than in control mice. The regional differences in density were detected by a more pronounced density in the lateral than in the medial and intermediate nuclei. Furthermore, Cav2.1 immunostaining also appeared in the torpedoes of Purkinje cell axons, which were apposed to large- or medium-sized deep cerebellar neurons. Those results suggest that altered functions of the Cav2.1 channel in rolling mice are involved in the torpedoes of Purkinje cell axons in the deep cerebellar nuclei, which may be related to the animal's motor incoordination.
Ca2+ channelopathy, Neuropathy, Swelling, Cerebellum, Ataxia
