RT Journal Article SR Electronic T1 LMTK3 Deficiency Causes Pronounced Locomotor Hyperactivity and Impairs Endocytic Trafficking JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 5927 OP 5937 DO 10.1523/JNEUROSCI.1621-13.2014 VO 34 IS 17 A1 Takeshi Inoue A1 Naosuke Hoshina A1 Takanobu Nakazawa A1 Yuji Kiyama A1 Shizuka Kobayashi A1 Takaya Abe A1 Toshifumi Yamamoto A1 Toshiya Manabe A1 Tadashi Yamamoto YR 2014 UL http://www.jneurosci.org/content/34/17/5927.abstract AB 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.