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首页> 外文期刊>BMC Neuroscience >Knockout of the circadian gene, Per2 , disrupts corticosterone secretion and results in depressive‐like behaviors and deficits in startle responses
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Knockout of the circadian gene, Per2 , disrupts corticosterone secretion and results in depressive‐like behaviors and deficits in startle responses

机译：截止昼夜昼夜基因，截断，扰乱皮质酮分泌，导致令人抑制的行为和惊吓反应的缺陷

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The Period Circadian Regulator 2 (Per2) gene is important for the modulation of circadian rhythms that influence biological processes. Circadian control of the hypothalamus-pituitary-adrenal (HPA) axis is critical for regulation of hormones involved in the stress response. Dysregulation of the HPA axis is associated with neuropsychiatric disorders. Therefore, it is important to understand how disruption of the circadian rhythm alters the HPA axis. One way to address this question is to delete a gene involved in regulating a central circadian gene such as Per2 in an animal model and to determine how this deletion may affect the HPA axis and behaviors that are altered when the HPA axis is dysregulated. To study this, corticosterone (CORT) levels were measured through the transition from light (inactive phase) to dark (active phase). Additionally, CORT levels as well as pituitary and adrenal mRNA expression were measured following a mild restraint stress. Mice were tested for depressive-like behaviors (forced swim test (FST)), acoustic startle response (ASR), and pre-pulse inhibition (PPI). The present results showed that Per2 knockout impacted CORT levels, mRNA expression, depressive-like behaviors, ASR and PPI. Unlike wild-type (WT) mice, Per2 knockout (Per2) mice showed no diurnal rise in CORT levels at the onset of the dark cycle. Per2?/? mice had enhanced CORT levels and adrenal melanocortin receptor 2 (Mc2R) mRNA expression following restraint. There were no changes in expression of any other pituitary or adrenal gene. In the FST, Per2?/? mice spent more time floating (less time struggling) than WT mice, suggesting increased depressive-like behaviors. Per2?/? mice had deficits in ASR and PPI startle responses compared to WT mice. In summary, these findings showed that disruption of the circadian system via Per2 gene deletion dysregulated the HPA stress axis and is subsequently correlated with increased depressive-like behaviors and deficits in startle response.
机译：周期昼夜节律调节剂2（PER2）基因对于调制影响生物过程的昼夜节律来说是重要的。昼夜垂体 - 垂体 - 肾上腺（HPA）轴的昼夜昼夜控制对于调节参与应力反应的激素至关重要。 HPA轴的失调与神经精神障碍有关。因此，重要的是要了解昼夜节律的破坏如何改变HPA轴。解决这个问题的一种方法是删除在动物模型中调节中央昼夜昼夜节律基因的基因，并确定该缺失如何影响HPA轴和当HPA轴被吸引时改变的行为。为此，通过从光（无活性相）到暗（活性相）的过渡测量皮质酮（皮质）水平。另外，在轻度约束应力后测量皮质水平和垂体和肾上腺mRNA表达。测试小鼠的抑郁样行为（强制游泳测试（FST）），声学惊吓响应（ASR）和预脉冲预抑制（PPI）。目前的结果表明，PER2敲除受影响的皮质水平，mRNA表达，抑郁的行为，ASR和PPI。与野生型（WT）小鼠不同，PER2敲除（PER2）小鼠在黑暗循环开始时显示了CORT水平的昼夜上升。 per2？/？小鼠具有增强的皮质水平和肾上腺素素受体2（MC2R）mRNA表达后抑制。任何其他垂体或肾上腺基因表达没有变化。在FST，PER2？/？小鼠花了更多的时间漂浮（减少时间）而不是WT小鼠，表明增加了抑郁的行为。 per2？/？与WT小鼠相比，小鼠在ASR和PPI Surrowes响应中具有缺陷。总之，这些发现表明，通过PER2基因缺失的昼夜性系统破坏了解HPA应力轴，随后与抑郁状行为和惊吓响应中的缺陷相关。

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