Prenatal dexamethasone exposure affects anxiety-like behaviour and neuroendocrine systems in an age-dependent manner
Prenatal dexamethasone exposure affects anxiety-like behaviour and neuroendocrine systems in an age-dependent manner
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DOI：
10.1016/j.neures.2007.12.005
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发表时间：
2008-04-01
影响因子：
2.9
通讯作者：
Suzuki, Hidenori
中科院分区：
文献类型：
--
作者：
Nagano, Masatoshi;Ozawa, Hitoshi;Suzuki, Hidenori
据报道，产前压力会改变中枢神经系统功能的发育。这种改变被认为部分是由于胎儿暴露于糖皮质激素增加引起的。为了阐明产前应激如何以年龄依赖性方式影响神经内分泌系统和行为，我们在妊娠第16-21天给孕鼠施用合成糖皮质激素地塞米松作为应激源，并检查雄性后代行为、下丘脑促肾上腺皮质激素释放因子mRNA表达、皮质酮反应和糖皮质激素受体表达的发育变化。产前地塞米松暴露降低了下丘脑促肾上腺皮质激素释放因子mRNA，并扰乱了产后4周（PW 4）后代对束缚应激的血浆皮质酮反应。相比之下，直到PW 10，增加焦虑样行为出现在地塞米松暴露的后代。与PW 10时获得焦虑样行为增加相关，PW 7和PW 10时地塞米松暴露后代杏仁核中糖皮质激素受体表达降低。因此，我们的纵向分析表明，产前暴露于糖皮质激素阻碍神经内分泌发育的后代在生命早期，这种干扰的结果在诱导增加焦虑样行为在成年期。(C)2007 Elsevier爱尔兰有限公司和日本神经科学学会。All rights reserved.
Prenatal stress has been reported to alter the development of the central nervous system functions. This alteration is thought to be partly caused by increased fetal exposure to glucocorticoid. To clarify how prenatal stress affects neuroendocrine systems and behaviour in an age-dependent manner, we administered a synthetic glucocorticoid, dexamethasone, as a stressor to pregnant rats at gestational days 16-21 and examined the developmental changes in behaviour, hypothalamic corticotropin-releasing factor mRNA expression, corticosterone response and glucocorticoid receptor expression in male offspring. Prenatal dexamethasone exposure decreased corticotropin-releasing factor mRNA in the hypothalamus and disturbed the plasma corticosterone response to restraint stress in the offspring at postnatal week 4 (PW4). In contrast, it was not until PW10 that increased anxiety-like behaviour emerged in the dexamethasone-exposed offspring. In association with the acquisition of increased anxiety-like behaviour at PW10, glucocorticoid receptor expression was decreased in the amygdala in dexamethasone-exposed offspring at PW7 and PW10. Thus, our longitudinal analysis suggests that prenatal exposure to glucocorticoid hampers neuroendocrinological development in the offspring during early life, and that this disturbance results in the induction of increased anxiety-like behaviour in adulthood. (C) 2007 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.