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  1. Academic Journal articles
  2. Yamamoto Unit

Lmtk3-KO Mice Display a Range of Behavioral Abnormalities and Have an Impairment in GluA1 Trafficking

https://oist.repo.nii.ac.jp/records/1170
https://oist.repo.nii.ac.jp/records/1170
e02a97ea-3a3e-40db-bef7-250d56a1fca7
Name / File License Actions
Neuroscience Neuroscience Montrose revision (clear copy)_with CC-BY-NC-ND license (915.0 kB)
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (http://creativecommons.org/Licenses/by-nc-nd/4.0/)
Item type 学術雑誌論文 / Journal Article(1)
PubDate 2020-02-10
Title
Title Lmtk3-KO Mice Display a Range of Behavioral Abnormalities and Have an Impairment in GluA1 Trafficking
Language en
Language
Language eng
Resource Type
Resource Type Identifier http://purl.org/coar/resource_type/c_6501
Resource Type journal article
Author Montrose, Kristopher

× Montrose, Kristopher

Montrose, Kristopher

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Kobayashi, Shizuka

× Kobayashi, Shizuka

Kobayashi, Shizuka

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Manabe, Toshiya

× Manabe, Toshiya

Manabe, Toshiya

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Yamamoto, Tadashi

× Yamamoto, Tadashi

Yamamoto, Tadashi

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Bibliographic Information en : Neuroscience

Volume Number 414, p. 154-167, Issue Date 2019-07-13
Abstract
Description Type Other
Description Accumulating evidence suggests that glutamatergic signaling and synaptic plasticity underlie one of a number of ways psychiatric disorders appear. The present study reveals a possible mechanism by which this occurs, through highlighting the importance of LMTK3, in the brain. Behavioral analysis of Lmtk3-KO mice revealed a number of abnormalities that have been linked to psychiatric disease such as hyper-sociability, PPI deficits and cognitive dysfunction. Treatment with clozapine suppressed these behavioral changes in Lmtk3-KO mice. As synaptic dysfunction is implicated in human psychiatric disease, we analyzed the LTP of Lmtk3-KO mice and found that induction is severely impaired. Further investigation revealed abnormalities in GluA1 trafficking after AMPA stimulation in Lmtk3-KO neurons, along with a reduction in GluA1 expression in the post-synaptic density. Therefore, we hypothesize that LMTK3 is an important factor involved in the trafficking of GluA1 during LTP, and that disruption of this pathway contributes to the appearance of behavior associated with human psychiatric disease in mice.
ISSN
Source Identifier Type ISSN
Source Identifier 0306-4522
ISSN
Source Identifier Type ISSN
Source Identifier 1873-7544
PubMedNo.
Relation Type isVersionOf
Identifier Type PMID
Related Identifier info:pmid/31310731
DOI
Relation Type isVersionOf
Identifier Type DOI
Related Identifier info:doi/10.1016/j.neuroscience.2019.06.033
Rights
Rights © 2019 IBRO. Published by Elsevier Ltd.
Resources
Related Title http://creativecommons.org/Licenses/by-nc-nd/4.0/
Related site
Identifier Type URI
Related Identifier https://www.sciencedirect.com/science/article/pii/S0306452219304506
Author's flag
Version Type AM
Version Type Resource http://purl.org/coar/version/c_ab4af688f83e57aa
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