The absence of the SOD1 gene causes abnormal monoaminergic neurotransmission and motivational impairment-like behavior in mice.
The absence of the SOD1 gene causes abnormal monoaminergic neurotransmission and motivational impairment-like behavior in mice.
复制标题
SOD1 基因的缺失会导致小鼠单胺能神经传递异常和动机障碍样行为。
DOI：
10.1080/10715762.2016.1234048
复制
发表时间：
2016
影响因子：
3.3
通讯作者：
Motohiko Takemura and Keiichiro Suzuki
中科院分区：
文献类型：
--
作者：
Daisaku Yoshihara;Noriko Fujiwara;Nobue Kitanaka;Junichi Kitanaka;Haruhiko Sakiyama;Hironobu Eguchi;Motohiko Takemura and Keiichiro Suzuki
铜/锌超氧化物歧化酶（SOD 1），一种主要的抗氧化酶，保护细胞免受氧化应激。我们在此报告的行为和神经生物学的变化之间的比较SOD 1敲除（KO）和野生型小鼠，试图评估SOD 1在脑功能中的作用。SOD 1基因敲除小鼠在梭箱学习和三室社交互动测试中表现出动机行为受损。在SOD 1基因敲除小鼠的大脑中也检测到高水平的多巴胺转运蛋白和5-羟色胺周转加速。这些发现表明，SOD 1缺乏干扰单胺能神经传递，导致动机行为减少。
Copper/zinc superoxide dismutase (SOD1), a primary anti-oxidative enzyme, protects cells against oxidative stress. We report herein on a comparison of behavioral and neurobiological changes between SOD1 knockout (KO) and wild-type mice, in an attempt to assess the role of SOD1 in brain functions. SOD1 KO mice exhibited impaired motivational behavior in both shuttle-box learning and three-chamber social interaction tests. High levels of dopamine transporter protein and an acceleration of serotonin turnover were also detected in the cerebrums of the SOD1 KO mice. These findings suggest that SOD1 deficiency disturbs monoaminergic neurotransmission leading to a decrease in motivational behavior.