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Updated: Apr 30, 2026

Gait Analysis of Age-dependent Motor Impairments in Mice with Neurodegeneration
Published on: June 18, 2018
LMTK3 deficiency causes pronounced locomotor hyperactivity and impairs endocytic trafficking
Takeshi Inoue1, Naosuke Hoshina, Takanobu Nakazawa
1Division of Oncology and Division of Neuronal Network, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan, Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan, Laboratory of Molecular Recognition, Graduate School of Arts and Sciences, Yokohama City University, Yokohama 236-0027, Japan, and Cell Signal Unit, Okinawa Institute of Science and Technology, Onna-son, Okinawa 904-0495, Japan.
Abstract:
LMTK3 belongs to the LMTK family of protein kinases that are predominantly expressed in the brain. Physiological functions of LMTK3 and other members of the LMTK family in the CNS remain unknown. In this study, we performed a battery of behavioral analyses using Lmtk3(-/-) mice and showed that these mice exhibit abnormal behaviors, including pronounced locomotor hyperactivity, reduced anxiety behavior, and decreased depression-like behavior. Concurrently, the dopamine metabolite levels and dopamine turnover rate are increased in the striata of Lmtk3(-/-) mice compared with wild-type controls. In addition, using cultured primary neurons from Lmtk3(-/-) mice, we found that LMTK3 is involved in the endocytic trafficking of N-methyl-d-aspartate receptors, a type of ionotropic glutamate receptor. Altered membrane traffic of the receptor in Lmtk3(-/-) neurons may underlie behavioral abnormalities in the mutant animals. Together, our data suggest that LMTK3 plays an important role in regulating locomotor behavior in mice.
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