Stress in utero alters neonatal stress-induced regulation of the synaptic plasticity proteins Arc and Egr1 in a sex-specific manner
Stress in utero alters neonatal stress-induced regulation of the synaptic plasticity proteins Arc and Egr1 in a sex-specific manner
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DOI：
10.1007/s00429-014-0889-3
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发表时间：
2016-01-01
影响因子：
3.1
通讯作者：
Braun, Katharina
中科院分区：
文献类型：
--
作者：
Groeger, Nicole;Bock, Joerg;Braun, Katharina
本研究在青少年大鼠调查了“两击模型”，以测试产前应激暴露（“第一击”）的突触可塑性立即早期基因Arc和Egr 1的调节响应于第二新生儿应激（“第二击”）在性别特异性的方式的影响。在21日龄时，将三个应激暴露动物组与未应激对照组（CON）进行比较：preS动物在妊娠最后三个月期间暴露于各种不可预测的应激源; postS动物在出生后第21天暴露于45分钟的束缚应激，preS/postS动物暴露于前两组所述的产前和产后应激的组合。postS组和pre-postS组在暴露于出生后应激源后2 h处死，雌雄各半。与我们的假设一致，我们检测到两种分析蛋白质的性别特异性应激敏感性。无论应激条件如何，雄性动物的Arc表达均未显示任何显著变化。与此相反，女性，这已预先暴露于产前压力，显示了“放大”弧上调响应产后压力（前/后S组）相比，无压力的控制，这可能反映了“致敏”的产前压力的影响。对于Egr 1，女性并没有表现出任何压力诱导的调节，无论压力条件，而在男性，这是预先暴露于产前压力，我们观察到的“保护”作用，产前压力对产后压力诱导的Egr 1表达下调（前/后S组），这可能表明，产前压力暴露可能会诱导“弹性”。
The present study in juvenile rats investigated a "two-hit model" to test the impact of prenatal stress exposure ("first hit") on the regulation of the synaptic plasticity immediate early genes Arc and Egr1 in response to a second neonatal stressor ("second hit") in a sex-specific manner. Three stress-exposed animal groups were compared at the age of 21 days in relation to unstressed controls (CON): preS animals were exposed to various unpredictable stressors during the last gestational trimester; postS animals were exposed to 45 min restraint stress at postnatal day 21, pre/postS animals were exposed to a combination of pre- and postnatal stress as described for the two previous groups. The postS and pre/postS groups were killed 2 h after exposure to the postnatal stressor, males and females were separately analyzed. In line with our hypothesis we detected sex-specific stress sensitivity for both analyzed proteins. Males did not show any significant changes in Arc expression irrespective of the stress condition. In contrast, females, which had been pre-exposed to prenatal stress, displayed an "amplified" Arc upregulation in response to postnatal stress (pre/postS group) compared to unstressed controls, which may reflect a "sensitization" effect of prenatal stress. For Egr1, the females did not show any stress-induced regulation irrespective of the stress condition, whereas in males, which were pre-exposed to prenatal stress, we observed a "protective" effect of prenatal stress on postnatal stress-induced downregulation of Egr1 expression (pre/postS group), which may indicate that prenatal stress exposure may induce "resilience".