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Title: TRPM2 confers susceptibility to social stress but is essential for behavioral flexibility
Authors: Andoh, Chihiro
Nishitani, Naoya
Hashimoto, Emina
Nagai, Yuma
Takao, Keizo
Miyakawa, Tsuyoshi
Nakagawa, Takayuki
Mori, Yasuo
Nagayasu, Kazuki
Shirakawa, Hisashi
Kaneko, Shuji
Author's alias: 安藤 千紘
西谷 直也
中川, 貴之
森, 泰生
永安, 一樹
白川, 久志
金子, 周司
Keywords: TRPM2
Stress resiliency
Behavioral inflexibility
Issue Date: 1-Feb-2019
Publisher: Elsevier B.V.
Journal title: Brain Research
Volume: 1704
Start page: 68
End page: 77
Abstract: Transient receptor potential melastatin 2 (TRPM2) is a Ca²⁺-permeable, nonselective cation channel and a member of the TRP channel superfamily that acts as a sensor of intracellular redox states. TRPM2 is widely distributed in many tissues and highly expressed in the brain, but the physiological roles of TRPM2 in the central nervous system remain unclear. In this study, TRPM2-deficient mice were examined in a series of behavioral tests. TRPM2-deficient mice did not significantly differ from wild-type littermates in muscle strength, light/dark transition test, rotarod, elevated plus maze, social interaction, prepulse inhibition, Y-maze, forced swim test, cued and contextual fear conditioning, and tail suspension test. In the Barnes circular maze, TRPM2-deficient mice learned the fixed escape box position at similar extent to wild-type littermates, suggesting normal reference memory. However, performance of the first reversal trial and probe test were significantly impaired in TRPM2-deficient mice. In the T-maze delayed alternation task, TRPM2 deficiency significantly reduced choice accuracy. These results indicate that TRPM2-deficient mice shows behavioral inflexibility. Meanwhile, social avoidance induced by repeated social defeat stress was significantly attenuated in TRPM2-deficient mice, suggesting that TRPM2 deficiency confers stress resiliency. Our findings indicate that TRPM2 plays an essential role in maintaining behavioral flexibility but it increases susceptibility to stress.
Rights: © 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/.
The full-text file will be made open to the public on 1 February 2020 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
URI: http://hdl.handle.net/2433/241623
DOI(Published Version): 10.1016/j.brainres.2018.09.031
PubMed ID: 30273551
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