Academic Thesis

Basic information

Name Katayama Keiichi
Belonging department
Occupation name
researchmap researcher code B000305947
researchmap agency Okayama University of Science

Title

Slitrk2 deficiency causes hyperactivity with altered vestibular function and serotonergic dysregulation.

Bibliography Type

 

Author

Kei-Ichi Katayama
Naoko Morimura
Katsunori Kobayashi
Danielle Corbett
Takehito Okamoto
Veravej G Ornthanalai
Hayato Matsunaga
Wakako Fujita
Yoshifumi Matsumoto
Takumi Akagi
Tsutomu Hashikawa
Kazuyuki Yamada
Niall P Murphy
Soichi Nagao
Jun Aruga

Summary

SLITRK2 encodes a transmembrane protein that modulates neurite outgrowth and synaptic activities and is implicated in bipolar disorder. Here, we addressed its physiological roles in mice. In the brain, the Slitrk2 protein was strongly detected in the hippocampus, vestibulocerebellum, and precerebellar nuclei-the vestibular-cerebellar-brainstem neural network including pontine gray and tegmental reticular nucleus. Slitrk2 knockout (KO) mice exhibited increased locomotor activity in novel environments, antidepressant-like behaviors, enhanced vestibular function, and increased plasticity at mossy fiber-CA3 synapses with reduced sensitivity to serotonin. A serotonin metabolite was increased in the hippocampus and amygdala, and serotonergic neurons in the raphe nuclei were decreased in Slitrk2 KO mice. When KO mice were treated with methylphenidate, lithium, or fluoxetine, the mood stabilizer lithium showed a genotype-dependent effect. Taken together, Slitrk2 deficiency causes aberrant neural network activity, synaptic integrity, vestibular function, and serotonergic function, providing molecular-neurophysiological insight into the brain dysregulation in bipolar disorders.

Magazine(name)

iScience

Publisher

 

Volume

25

Number Of Pages

7

StartingPage

104604

EndingPage

104604

Date of Issue

2022-07-15

Referee

Exist

Invited

 

Language

English

Thesis Type

Research papers (academic journals)

ISSN

 

DOI

10.1016/j.isci.2022.104604

NAID

 

PMID

 

J-GLOBAL ID

 

arXiv ID

 

ORCID Put Code

 

DBLP ID