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Sema4D/CD100 Deficiency Leads to Superior Performance in Mouse Motor Behavior

Published online by Cambridge University Press:  02 December 2014

Kazunori Yukawa*
Affiliation:
Department of Physiology, Faculty of Pharmacy, Meijo University, Tempaku-ku, Nagoya
Tetsuji Tanaka
Affiliation:
Department of Obstetrics & Gynecology, Wakayama Medical University, Wakayama
Noriko Takeuchi
Affiliation:
Department of Physiology, Faculty of Pharmacy, Meijo University, Tempaku-ku, Nagoya
Hiroyuki Iso
Affiliation:
Department of Behavioral Science, Hyogo College of Medicine, Nishinomiya
Li Li
Affiliation:
Department of Obstetrics & Gynecology, Wakayama Medical University, Wakayama
Akira Kohsaka
Affiliation:
Department of Obstetrics & Physiology, Wakayama Medical University, Wakayama
Hidefumi Waki
Affiliation:
Department of Obstetrics & Physiology, Wakayama Medical University, Wakayama
Masayasu Miyajima
Affiliation:
Department of Obstetrics & Animal Facility, Wakayama Medical University, Wakayama
Masanobu Maeda
Affiliation:
Department of Obstetrics & Physiology, Wakayama Medical University, Wakayama
Hitoshi Kikutani
Affiliation:
Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan
Atsushi Kumanogoh
Affiliation:
Department of Obstetrics & Physiology, Wakayama Medical University, Wakayama Department of Immunopathology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan
*
Department of Physiology, Faculty of Pharmacy, Meijo University, 150 Yagotoyama, Tempaku-ku, Nagoya 468-8503, Japan
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Abstract

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Background:

Sema4D/CD100 is a type of class 4 semaphorin, exhibiting crucial rôles in growth cone guidance in developing neurons. Sema4D is widely expressed throughout the central nervous system in embryonic mouse brain, and is selectively localized to oligodendrocytes and myelin in the postnatal brain. However, direct evidence of the actual involvement of Sema4D in the neuronal network development crucial for neurobehavioral performance is still lacking. The present study therefore examined whether Sema4D deficiency leads to abnormal behavioral development.

Methods:

Both wild-type and Sema4D-deficient mice were subjected to behavioral analyses including open-field, adhesive tape removal, rotarod tests and a water maze task.

Results:

Open-field tests revealed increased locomotor activity in Sema4D-deficient mice with less percentage of time spent in the center of the field. In both the adhesive tape removal and rotarod tests, which examine motor coordination and balance, Sema4D-deficient mice showed significantly superior performance, suggesting facilitated motor behavior. Both Sema4D-deficient and wild-type mice successfully learnt the water maze task, locating a hidden escape platform, and also showed precise memory for the platform position in probe tests. However, the swimming speed of Sema4D-deficient mice was significantly faster than that of wild-type mice, providing further evidence of their accelerated motor behavior.

Conclusion:

Our mouse behavioral analyses revealed enhanced motor activity in Sema4D-deficient mice, suggesting the crucial involvement of Sema4D in the neurodevelopmental processes of the central structures mediating motor behavior in mice.

Type
Original Article
Copyright
Copyright © The Canadian Journal of Neurological 2009

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