Heightened aggressive behavior in mice deficient in aldo-keto reductase 1a (Akr1a).
Heightened aggressive behavior in mice deficient in aldo-keto reductase 1a (Akr1a).
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醛酮还原酶 1a (Akr1a) 缺陷小鼠的攻击行为增强。
DOI：
10.1016/j.bbr.2016.11.038
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发表时间：
2017
影响因子：
2.7
通讯作者：
Junichi Fujii
中科院分区：
文献类型：
--
作者：
Takujiro Homma;Ryusuke Akihara;Satoshi Okano;Mototada Shichiri;Yasukazu Yoshida;Ken-ichi Yamada;Satoshi Miyata;Osamu Nakajima;Junichi Fujii
醛还原酶（Akr 1a）参与抗坏血酸（阿萨）的合成，而抗坏血酸可能在社会行为中发挥作用。在本研究中，我们从雄性间攻击的角度对合成约为野生型小鼠10%的阿萨的Akr 1a缺陷型（Akr 1a −/−）小鼠进行了分析。居民入侵者测试的使用显示，Akr 1a −/−小鼠比野生型对照小鼠表现出更多的攻击性表型。然而，出乎意料的是，口服额外的阿萨未能减少Akr 1a −/−小鼠的攻击行为，这表明攻击性的增强与阿萨的生物合成无关。研究结果还表明，在缺乏Akr 1a的情况下，小鼠的血浆皮质酮水平增加，而不是血清素和睾酮，这表明小鼠受到高度压力。这些结果表明，Akr 1a可能参与类固醇和其他含羰基化合物的代谢，因此，Akr 1a的缺乏通过代谢途径的功能障碍导致攻击性增强。
Aldehyde reductase (Akr1a) is involved in the synthesis of ascorbic acid (AsA) which may play a role in social behavior. In the current study, we performed analyses on Akr1a-deficient (Akr1a−/−) mice that synthesize about 10% as much AsA as wild-type mice from the viewpoint of intermale aggression. The use of the resident-intruder test revealed that the Akr1a−/−mice exhibited more aggressive phenotypes than wild-type control mice. Unexpectedly, however, the oral administration of additional AsA failed to reduce the aggressive behavior of Akr1a−/−mice, suggesting that the heightened aggression was independent of AsA biosynthesis. The findings also show that the plasma levels of corticosterone, but not serotonin and testosterone, were increased in the absence of Akr1a in mice, suggesting that the mice were highly stressed. These results suggest that Akr1a might be involved in the metabolism of steroids and other carbonyl-containing compounds and, hence, the absence of Akr1a results in heightened aggression via a malfunction in a metabolic pathway.