Dietary habits are important factors which affect metabolic homeostasis and the development of emotion. We have previously shown that long-term powdered diet feeding in mice increases spontaneous locomotor activity and social interaction (SI) time. Moreover, that diet causes changes in the dopaminergic system, especially increased dopamine turnover and decreased dopamine D4 receptor signals in the frontal cortex. Although the increased SI time indicates low anxiety, the elevated plus maze (EPM) test shows anxiety-related behavior and impulsive behavior. In this study, we investigated whether the powdered diet feeding causes changes in anxiety-related behavior. Mice fed a powdered diet for 17 weeks from weaning were compared with mice fed a standard diet (control). The percentage (%) of open arm time and total number of arm entries were increased in powdered diet-fed mice in the EPM test. We also examined the effects of diazepam, benzodiazepine anti-anxiety drug, bicuculline, GABA-A receptor antagonist, methylphenidate, dopamine transporter (DAT) and noradrenaline transporter (NAT) inhibitor, atomoxetine, selective NAT inhibitor, GBR12909, selective DAT inhibitor, and PD168077, selective dopamine D4 receptor agonist, on the changes of the EPM in powdered diet-fed mice. Methylphenidate and atomoxetine are clinically used to treat attention deficit/hyperactivity disorder (ADHD) symptoms. The % of open arm time in powdered diet-fed mice was decreased by treatments of atomoxetine, methylphenidate and PD168077. Diazepam increased the % of open arm time in control diet-fed mice, but not in powdered diet-fed mice. The powdered diet feeding induced a decrease in GABA transaminase, GABA metabolic enzymes, in the frontal cortex. Moreover, the powdered diet feeding induced an increase in NAT expression, but not DAT expression, in the frontal cortex. These results suggest that the long-term powdered diet feeding may cause low anxiety or impulsivity, possibly via noradrenergic and/or dopaminergic, and GABAAergic mediations and increase the risk for onset of ADHD-like behaviors.

中文翻译：

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儿茶酚胺能和GABA能量介导参与长期粉状饮食喂养小鼠的焦虑相关行为。

饮食习惯是影响代谢稳态和情绪发展的重要因素。先前我们已经表明，长期给小鼠粉状饮食喂养会增加自发运动能力和社交互动（SI）时间。此外，该饮食会引起多巴胺能系统的变化，尤其是额叶皮层中多巴胺周转率增加和多巴胺D4受体信号减少。尽管增加的SI时间表明焦虑程度较低，但是高架迷宫（EPM）测试显示出与焦虑相关的行为和冲动行为。在这项研究中，我们调查了粉状饮食是否引起焦虑相关行为的改变。断奶后喂食粉状饮食17周的小鼠与喂食标准饮食的小鼠（对照）进行比较。在EPM测试中，粉状饮食喂养的小鼠的张开双臂时间的百分比（％）和手臂进入的总数增加了。我们还检查了地西epa，苯二氮卓抗焦虑药，比库林，GABA-A受体拮抗剂，哌醋甲酯，多巴胺转运蛋白（DAT）和去甲肾上腺素转运蛋白（NAT）抑制剂，阿托西汀，选择性NAT抑制剂，GBR12909，选择性DAT抑制剂和PD168077，选择性多巴胺D4受体激动剂，对粉状饮食喂养小鼠中EPM的变化。哌醋甲酯和托莫西汀在临床上用于治疗注意力不足/多动症（ADHD）症状。用阿托西汀，哌醋甲酯和PD168077处理可降低粉状饮食喂养小鼠的开臂时间百分比。地西p增加了对照组饮食喂养小鼠的开臂时间百分比，但没有增加粉末饮食喂养小鼠的开臂时间百分比。饲料中的粉状饲料诱导了额叶皮质中GABA转氨酶，GABA代谢酶的减少。而且，粉状饮食喂养引起额叶皮层中NAT表达的增加，而不是DAT表达的增加。这些结果表明，长期的粉状饮食喂养可能会导致低焦虑或冲动，可能是通过去甲肾上腺素能和/或多巴胺能和GABAA能介导的，并增加了多动症样行为发作的风险。