Maternal deprivation potentiates pituitary-adrenal stress responses in infant rats.

Maternal deprivation potentiates pituitary-adrenal stress responses in infant rats.
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DOI:
10.1037/0735-7044.102.5.692
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发表时间:
1988-10
影响因子:
1.9
通讯作者:
M. Stanton;Yvonne R. Gutierrez;S. Levine
M. Stanton;Yvonne R. Gutierrez;S. Levine
中科院分区:
医学4区
文献类型:
--
作者:
M. Stanton;Yvonne R. Gutierrez;S. Levine

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在三个实验中,我们检测了母性剥夺对12、16和20日龄大鼠幼鼠对新奇应激的垂体-肾上腺反应的影响。幼鼠要么被单独剥夺在加热的孵化器中,要么与它们的母亲一起留在家里的巢中,然后测试它们在一个新的测试场所暴露30分钟后的皮质类固醇反应(新奇压力)。在实验1中,我们发现应激反应的大小是剥夺间隔的正加速函数。被剥夺1小时后应激反应没有增加,被剥夺8小时后应激反应略有增加,被剥夺24小时后应激反应显著增加。在实验2中,我们询问应激反应的增强是由母体还是剥夺过程中的营养成分引起的。幼犬在四种治疗条件中的一种下进行测试,这四种治疗条件由2(母体剥夺与未剥夺)x 2(营养剥夺与未剥夺)因子设计组成。在12日龄和16日龄时,应激反应的增强可以追溯到缺乏母亲的照顾,而不是营养。在20日龄时,母体和营养剥夺均导致应激反应增强。实验3的结果表明,这种影响至少部分是由肾上腺皮质对ACTH的敏感性增加介导的,因为皮质类固醇对外源性ACTH的反应也会因母体剥夺而增加。这些发现增加了越来越多的文献,支持母亲调节婴儿生理的概念。他们还支持该实验室先前的报告,即在大鼠断奶前,垂体-肾上腺系统的抑制是由母体变量调节的。
In three experiments we examined the effect of maternal deprivation on the pituitary-adrenal response of 12-, 16- and 20-day-old rat pups to novelty stress. Infant rats were either deprived individually in heated incubators or left in the home nest with their mother and then tested for their corticosteroid response to 30-min exposure to a novel test arena (novelty-stress). In Experiment 1 we showed that the magnitude of the stress response was a positively accelerated function of the deprivation interval. Stress responses were not increased after 1 hour of deprivation, were modestly increased after 8 hours of deprivation, and were dramatically increased after 24 hours of deprivation. In Experiment 2 we asked whether potentiation of the stress response resulted from the maternal or the nutritive components of the deprivation procedure. Pups were tested under one of four treatment conditions formed by a 2 (Maternally Deprived vs. Nondeprived) x 2 (Nutritively Deprived vs. Nondeprived) factorial design. At 12 and 16 days of age, potentiation of the stress response was traced to the absence of maternal care and not nutrients. At 20 days of age, both maternal and nutritive deprivation contributed to the potentiated stress response. The results of Experiment 3 showed that this effect was mediated, at least in part, by increased adrenocortical sensitivity to ACTH, because the corticosteroid response to exogenous ACTH administration was also increased by maternal deprivation. These findings add to a growing body of literature that supports the concept of maternal regulation of infant physiology. They also support previous reports from this laboratory indicating that suppression of the pituitary-adrenal system is modulated by maternal variables during the preweaning period in the rat.