Skip to main content

Main menu

  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE

User menu

  • Log out
  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • Log out
  • Log in
  • My Cart
Journal of Neuroscience

Advanced Search

Submit a Manuscript
  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE
PreviousNext
Articles, Cellular/Molecular

LMTK3 Deficiency Causes Pronounced Locomotor Hyperactivity and Impairs Endocytic Trafficking

Takeshi Inoue, Naosuke Hoshina, Takanobu Nakazawa, Yuji Kiyama, Shizuka Kobayashi, Takaya Abe, Toshifumi Yamamoto, Toshiya Manabe and Tadashi Yamamoto
Journal of Neuroscience 23 April 2014, 34 (17) 5927-5937; https://doi.org/10.1523/JNEUROSCI.1621-13.2014
Takeshi Inoue
1Division of Oncology and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Naosuke Hoshina
1Division of Oncology and
5Cell Signal Unit, Okinawa Institute of Science and Technology, Onna-son, Okinawa 904-0495, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Takanobu Nakazawa
1Division of Oncology and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yuji Kiyama
2Division of Neuronal Network, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Shizuka Kobayashi
2Division of Neuronal Network, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Takaya Abe
3Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Toshifumi Yamamoto
4Laboratory of Molecular Recognition, Graduate School of Arts and Sciences, Yokohama City University, Yokohama 236-0027, Japan, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Toshiya Manabe
2Division of Neuronal Network, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Tadashi Yamamoto
1Division of Oncology and
5Cell Signal Unit, Okinawa Institute of Science and Technology, Onna-son, Okinawa 904-0495, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

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.

  • endocytosis
  • hyperactivity
  • LMTK
  • locomotor
  • membrane trafficking
View Full Text
Back to top

In this issue

The Journal of Neuroscience: 34 (17)
Journal of Neuroscience
Vol. 34, Issue 17
23 Apr 2014
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by author
  • Advertising (PDF)
  • Ed Board (PDF)
Email

Thank you for sharing this Journal of Neuroscience article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
LMTK3 Deficiency Causes Pronounced Locomotor Hyperactivity and Impairs Endocytic Trafficking
(Your Name) has forwarded a page to you from Journal of Neuroscience
(Your Name) thought you would be interested in this article in Journal of Neuroscience.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
View Full Page PDF
Citation Tools
LMTK3 Deficiency Causes Pronounced Locomotor Hyperactivity and Impairs Endocytic Trafficking
Takeshi Inoue, Naosuke Hoshina, Takanobu Nakazawa, Yuji Kiyama, Shizuka Kobayashi, Takaya Abe, Toshifumi Yamamoto, Toshiya Manabe, Tadashi Yamamoto
Journal of Neuroscience 23 April 2014, 34 (17) 5927-5937; DOI: 10.1523/JNEUROSCI.1621-13.2014

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Respond to this article
Request Permissions
Share
LMTK3 Deficiency Causes Pronounced Locomotor Hyperactivity and Impairs Endocytic Trafficking
Takeshi Inoue, Naosuke Hoshina, Takanobu Nakazawa, Yuji Kiyama, Shizuka Kobayashi, Takaya Abe, Toshifumi Yamamoto, Toshiya Manabe, Tadashi Yamamoto
Journal of Neuroscience 23 April 2014, 34 (17) 5927-5937; DOI: 10.1523/JNEUROSCI.1621-13.2014
Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Introduction
    • Materials and Methods
    • Results
    • Discussion
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Keywords

  • endocytosis
  • hyperactivity
  • LMTK
  • locomotor
  • membrane trafficking

Responses to this article

Respond to this article

Jump to comment:

No eLetters have been published for this article.

Related Articles

Cited By...

More in this TOC Section

Articles

  • Memory Retrieval Has a Dynamic Influence on the Maintenance Mechanisms That Are Sensitive to ζ-Inhibitory Peptide (ZIP)
  • Neurophysiological Evidence for a Cortical Contribution to the Wakefulness-Related Drive to Breathe Explaining Hypocapnia-Resistant Ventilation in Humans
  • Monomeric Alpha-Synuclein Exerts a Physiological Role on Brain ATP Synthase
Show more Articles

Cellular/Molecular

  • CXCL12 Engages Cortical Inhibitory Neurons to Enhance Dendritic Spine Plasticity and Structured Network Activity
  • Atypical Cadherin FAT2 Is Required for Synaptic Integrity and Motor Behaviors
  • Sex Differences in Histamine Regulation of Striatal Dopamine
Show more Cellular/Molecular
  • Home
  • Alerts
  • Follow SFN on BlueSky
  • Visit Society for Neuroscience on Facebook
  • Follow Society for Neuroscience on Twitter
  • Follow Society for Neuroscience on LinkedIn
  • Visit Society for Neuroscience on Youtube
  • Follow our RSS feeds

Content

  • Early Release
  • Current Issue
  • Issue Archive
  • Collections

Information

  • For Authors
  • For Advertisers
  • For the Media
  • For Subscribers

About

  • About the Journal
  • Editorial Board
  • Privacy Notice
  • Contact
  • Accessibility
(JNeurosci logo)
(SfN logo)

Copyright © 2025 by the Society for Neuroscience.
JNeurosci Online ISSN: 1529-2401

The ideas and opinions expressed in JNeurosci do not necessarily reflect those of SfN or the JNeurosci Editorial Board. Publication of an advertisement or other product mention in JNeurosci should not be construed as an endorsement of the manufacturer’s claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in JNeurosci.