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Basal Ganglia

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Effect of Caspr3 deficiency on mouse behavior

  • P1-147
  • 平田 晴菜 / Haruna Hirata:1 高橋 阿貴 / Aki Takahashi:2 渡邉 和忠 / Kazutada Watanabe:1,3 小出 剛 / Tsuyoshi Koide:2 霜田 靖 / Yasushi Shimoda:1 
  • 1:長岡技術科学大学・生物系 / Dept Bioeng, Nagaoka Univ Tech, Niigata, Japan  2:国立遺伝学研究所・マウス開発研究室 / Mouse Genomics Resource Lab, Natl Inst Genetics, Shizuoka, Japan 3:長岡工業高等専門学校 / Nagaoka Natl Coll Tech, Niigata, Japan 

Caspr3 (Contactin associated protein-like 3, Cntnap3) is a neural cell adhesion molecule belonging to Caspr family which is composed of five members: Caspr, Caspr2, Caspr3, Caspr4 and Caspr5. It has been demonstrated that Caspr and Caspr2 play essential roles in formation and maintenance of myelinated nerves. We have recently shown that Caspr3 is expressed during the first to third postnatal weeks in the mouse basal ganglia including the striatum, external segment of the globus pallidus, subthalamic nucleus, substantia nigra. In the striatum, Caspr3 is expressed in a subpopulation of projection neurons that are called medium spiny neurons (MSNs). It is suggested that Caspr3 may be involved in the formation and function of the basal ganglia, but a physiological role of Caspr3 remains largely unknown. Here, we performed behavioral analysis of Caspr3-deficient mice to explore the role for Caspr3 in basal ganglia functions. To evaluate motor coordination and motor learning, an accelerating rotarod test was performed for five consecutive days. In the first two days, motor performance and learning efficiency of Caspr3-deficient mice were significantly less than the wild type mice. However, there were no differences in motor coordination and muscle strength between the wild-type and Caspr3-deficient mice. These results suggest that motor learning was impaired in Caspr3-deficient mice. Striatal synaptic plasticity is associated with motor learning. In addition, MSNs exhibit stereotypical changes in dendritic arborization during the second postnatal week when Caspr3 expression reaches its maximum level. Taken together, there is a possibility that behavioral abnormalities in Caspr3-deficient mice might result from aberration of neuronal morphology and synaptic plasticity in the striatum.

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