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Akt2 Deficiency is Associated with Anxiety and Depressive Behavior in Mice

机译：Akt2缺乏症与小鼠焦虑和抑郁行为有关

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biBackground /i/bThe economic burden associated with major depressive disorder and anxiety disorders render both disorders the most common and debilitating psychiatric illnesses. To date, the exact cellular and molecular mechanisms underlying the pathophysiology, successful treatment and prevention of these highly associated disorders have not been identified. Akt2 is a key protein in the phosphatidylinositide-3 (PI3K) / glycogen synthase 3 kinase (GSK3) signaling pathway, which in turn is involved in brain-derived neurotrophic factor (BDNF) effects on fear memory, mood stabilisation and action of several antidepressant drugs. The present study thus explored the impact of Akt2 on behaviour of mice. biMethods /i/bBehavioural studies (Open-Field, Light-Dark box, O-Maze, Forced Swimming Test, Emergence Test, Object Exploration Test, Morris Water Maze, Radial Maze) have been performed with Akt2 knockout mice (iakt/isupi-/-/i/sup) and corresponding wild type mice (iakt/isupi+/+/i/sup). biResults /i/bAnxiety and depressive behavior was significantly higher in iakt/isupi-/-/i/sup than in iakt/isupi+/+/i/sup mice. The iakt/isupi-/-/i/sup mice were cognitively unimpaired but displayed increased anxiety in several behavioral tests (O-Maze test, Light-Dark box, Open Field test). Moreover, iakt/isupi-/-/i/sup mice spent more time floating in the Forced Swimming test, which is a classical feature of experimental depression. biConclusion /i/bAkt2 might be a key factor in the pathophysiology of depression and anxiety.
机译：背景 与重度抑郁症和焦虑症相关的经济负担使这两种疾病均成为最常见且使人衰弱的精神疾病。迄今为止，尚未确定这些高度相关的疾病的病理生理学，成功的治疗和预防的确切细胞和分子机制。 Akt2是磷脂酰肌醇3（PI3K）/糖原合酶3激酶（GSK3）信号传导途径中的关键蛋白，其又参与脑源性神经营养因子（BDNF）对恐惧记忆，情绪稳定和几种抗抑郁药的作用。毒品。因此，本研究探讨了Akt2对小鼠行为的影响。 方法 行为学研究（开放视野，明暗盒子，O型迷宫，强迫游泳测试，紧急情况测试，物体探索测试，莫里斯水迷宫，径向迷宫）有用Akt2基因敲除小鼠（ akt -/- ）和相应的野生型小鼠（ akt + / + ）。 结果 akt -/- 的焦虑和抑郁行为明显高于 akt + / + 小鼠。 akt -/- 小鼠在认知上没有受损，但是在一些行为测试（O-迷宫测试，浅色暗框，打开实地测试）。此外， akt -/- 小鼠在强迫游泳测试中花费了更多的时间，这是实验性抑郁症的经典特征。 结论 Akt2可能是抑郁和焦虑症的病理生理学的关键因素。

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