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首页> 美国卫生研究院文献>Translational Psychiatry >Anxiety- rather than depression-like behavior is associated with adult neurogenesis in a female mouse model of higher trait anxiety- and comorbid depression-like behavior
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Anxiety- rather than depression-like behavior is associated with adult neurogenesis in a female mouse model of higher trait anxiety- and comorbid depression-like behavior

机译：在具有较高性状焦虑和共病抑郁样行为的雌性小鼠模型中焦虑而非抑郁样行为与成年神经发生有关

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Adult neurogenesis has been implicated in affective disorders and the action of antidepressants (ADs) although the functional significance of this association is still unclear. The use of animal models closely mimicking human comorbid affective and anxiety disorders seen in the majority of patients should provide relevant novel information. Here, we used a unique genetic mouse model displaying higher trait anxiety (HAB) and comorbid depression-like behavior. We demonstrate that HABs have a lower rate of hippocampal neurogenesis and impaired functional integration of newly born neurons as compared with their normal anxiety/depression-like behavior (NAB) controls. In HABs, chronic treatment with the AD fluoxetine alleviated their higher depression-like behavior and protected them from relapse for 3 but not 7 weeks after discontinuation of the treatment without affecting neurogenesis. Similar to what has been observed in depressed patients, fluoxetine treatment induced anxiogenic-like effects during the early treatment phase in NABs along with a reduction in neurogenesis. On the other hand, treatment with AD drugs with a particularly strong anxiolytic component, namely the neurokinin-1-receptor-antagonist L-822 429 or tianeptine, increased the reduced rate of neurogenesis in HABs up to NAB levels. In addition, challenge-induced hypoactivation of dentate gyrus (DG) neurons in HABs was normalized by all three drugs. Overall, these data suggest that AD-like effects in a psychopathological mouse model are commonly associated with modulation of DG hypoactivity but not neurogenesis, suggesting normalization of hippocampal hypoactivity as a neurobiological marker indicating successful remission. Finally, rather than to higher depression-related behavior, neurogenesis seems to be linked to pathological anxiety.
机译：成人神经发生与情感障碍和抗抑郁药（ADs）的作用有关，尽管这种关联的功能意义尚不清楚。使用动物模型来模仿大多数患者所见的人类合并症情感和焦虑症应提供相关的新颖信息。在这里，我们使用了独特的遗传小鼠模型，该模型显示出较高的性格焦虑（HAB）和共病的抑郁样行为。我们证明，与其正常的焦虑/抑郁样行为（NAB）对照相比，HABs的海马神经发生率较低，新生神经元的功能整合受损。在HAB中，用氟西汀长期治疗可减轻其较高的抑郁样行为，并在停止治疗后3至7周内使其免受复发的影响，而不会影响神经发生。与在抑郁症患者中观察到的情况相似，氟西汀治疗在NAB的早期治疗阶段诱导了类似血管生成的作用，并减少了神经发生。另一方面，用具有特别强抗焦虑成分的AD药物（即神经激肽1受体拮抗剂L-822 429或tianeptine）治疗，可使HABs的神经发生率降低至NAB水平。此外，所有三种药物均能使挑战性刺激引起的HABs中齿状回（DG）神经元的过度活化。总体而言，这些数据表明，精神病理学小鼠模型中的AD样效应通常与DG机能减退的调节相关，但与神经发生无关，这表明海马体机能减退正常化是一种神经生物学标记，表明成功缓解。最后，神经发生似乎与病理性焦虑有关，而不是与抑郁症相关的高行为有关。

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