characteristics of gait ataxia in δ2 glutamate receptor mutant mice, ho15j特征的步态共济失调δ2谷氨酸受体突变小鼠,ho15j.pdfVIP

Characteristics of Gait Ataxia in d2 Glutamate Receptor Mutant Mice, ho15J 1 1 2 1 2,3 1,3 Eri Takeuchi , Yamato Sato , Eriko Miura , Hiroshi Yamaura , Michisuke Yuzaki , Dai Yanagihara * 1 Graduate School of Arts and Sciences, The University of Tokyo, Komaba, Meguro-ku, Tokyo, Japan, 2 Department of Physiology, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan, 3 Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Chiyoda-ku, Tokyo, Japan Abstract The cerebellum plays a fundamental, but as yet poorly understood, role in the control of locomotion. Recently, mice with gene mutations or knockouts have been used to investigate various aspects of cerebellar function with regard to locomotion. Although many of the mutant mice exhibit severe gait ataxia, kinematic analyses of limb movements have been performed in only a few cases. Here, we investigated locomotion in ho15J mice that have a mutation of the d2 glutamate receptor. The cerebellum of ho15J mice shows a severe reduction in the number of parallel fiber-Purkinje synapses compared with wild-type mice. Analysis of hindlimb kinematics during treadmill locomotion showed abnormal hindlimb movements characterized by excessive toe elevation during the swing phase, and by severe hyperflexion of the ankles in ho15J mice. The great trochanter heights in ho15J mice were lower than in wild-type mice throughout the step cycle. However, there were no significant differences in various temporal parameters between ho15J and wild-type mice. We suggest that dysfunction of the cerebellar neuronal