Alterations in amygdala-prefrontal circuits in infants exposed to prenatal maternal depression.

Alterations in amygdala-prefrontal circuits in infants exposed to prenatal maternal depression.
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DOI:
10.1038/tp.2016.146
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发表时间:
2016-11-01
影响因子:
6.8
通讯作者:
Monk C
Monk C
中科院分区:
医学1区
文献类型:
--
作者:
Posner J;Cha J;Roy AK;Peterson BS;Bansal R;Gustafsson HC;Raffanello E;Gingrich J;Monk C

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产前暴露于母亲抑郁症是常见的,并使后代处于发展一系列神经精神疾病的风险之中。尽管其患病率和不利的协会,产前母亲抑郁症(PMD)赋予风险的神经生物学过程仍然知之甚少。母亲的情绪和胎儿的行为进行了评估之间的34和37孕周。采用静息态功能磁共振成像(fMRI)和弥散MRI,我们检查了64名婴儿(平均年龄=5.8±1.7周)的杏仁核-前额叶回路的功能和结构连接(n=20)和(n=44)在子宫内暴露于PMD。静息功能磁共振成像和弥散磁共振成像都表明PMD暴露婴儿的杏仁核-前额叶连接不典型:静息功能磁共振成像显示杏仁核和背侧前额叶皮质(PFC)之间的反向或负向功能连接增加,双侧,和扩散MRI表明右杏仁核和右腹侧PFC之间的结构连接减少。频谱动态因果模型支持这些发现,表明杏仁核改变-PMD暴露婴儿的PFC有效(或定向)连接最后,路径分析支持一个机械帐户PMD的第三个三个月的胎儿行为:PMD改变杏仁核PFC连接,这反过来又与增加胎儿心率反应性在子宫内扰动。这些数据表明,成熟和协调的中枢和外周生理改变产前暴露于母亲抑郁症。据我们所知,这是第一个研究直接关联婴儿MRI测量与行为胎儿心率反应,并支持PMD相关的杏仁核-PFC电路的发展变化与未来的神经行为成熟的假设。
Prenatal exposure to maternal depression is common and puts offspring at risk for developing a range of neuropsychiatric disorders. Despite its prevalence and adverse associations, neurobiological processes by which prenatal maternal depression (PMD) confers risk remain poorly understood. Maternal mood and fetal behavior were assessed between 34 and 37 gestational weeks. Using resting-state functional magnetic resonance imaging (fMRI) and diffusion MRI, we examined functional and structural connectivity within amygdala–prefrontal circuits in 64 infants (mean age=5.8±1.7 weeks) with (n=20) and without (n=44) in utero exposure to PMD. Resting fMRI and diffusion MRI both indicated atypical amygdala–prefrontal connectivity in PMD-exposed infants: Resting fMRI indicated increased inverse, or negative, functional connectivity between the amygdala and the dorsal prefrontal cortex (PFC), bilaterally, and diffusion MRI indicated decreased structural connectivity between the right amygdala and the right ventral PFC. Spectral dynamic causal modeling supported these findings suggesting altered amygdala–PFC effective (or directed) connectivity in PMD-exposed infants. Last, path analyses supported a mechanistic account relating PMD to a third-trimester fetal behavior: PMD alters amygdala–PFC connectivity, which in turn, is associated with an increase in fetal heart rate reactivity to in utero perturbation. These data suggest that the maturation and coordination of central and peripheral physiology are altered by prenatal exposure to maternal depression. To the best of our knowledge, this is the first study to directly associate infant MRI measures with a behavior—fetal heart rate response, and supports hypotheses that PMD-associated variations in the development of amygdala–PFC circuits are relevant for future neurobehavioral maturation.