Early Attachment Disruption, Inflammation, and Vulnerability for Depression in Rodent and Primate Models
Early Attachment Disruption, Inflammation, and Vulnerability for Depression in Rodent and Primate Models
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DOI：
10.3389/fnbeh.2018.00314
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发表时间：
2019-01-07
影响因子：
3
通讯作者：
Deak, Terrence
中科院分区：
文献类型：
--
作者：
Hennessy, Michael B.;Schiml, Patricia A.;Deak, Terrence
在非人类灵长类动物上的早期实验确定了子女依恋中断和抑郁样结果之间的关系。随后在大鼠和小鼠身上进行的研究有助于将抑郁样结果与母亲行为障碍联系起来。依恋中断的另一个方面，即依恋对象本身的缺失，可能会在另一种不同的实验室啮齿动物-豚鼠身上进行更有效的研究。在这里，我们讨论使用豚鼠进行这项工作的基本原理。然后，我们回顾了豚鼠的研究，这些研究提供了炎症机制的证据，这些机制既介导了分离过程中的抑郁样行为，也调节了应激反应的敏化，如被认为会导致晚年更容易患抑郁症。最后，我们讨论了最近在成年猴子身上进行的补充工作，这些工作表明从豚鼠实验中得出的广泛原则可以跨物种推广。总体而言，这些发现为人类的研究提供了实验支持，这些研究表明，炎症机制与依恋中断和其他形式的早期应激后压力反应增强和抑郁的易感性的发展有关。具体地说，这些发现表明，炎症机制可能启动了一系列潜在的过程，这些过程介导了后来压力反应的增强，从而导致了抑郁症的易感性。
Early experiments in nonhuman primates established the relation between disruption of filial attachment and depressive-like outcomes. Subsequent studies in rats and mice have been instrumental in linking depressive-like outcomes to disturbances in maternal behavior. Another aspect of attachment disruption, absence of the attachment object per se, may be studied more effectively in a different laboratory rodent-the guinea pig. Here, we discuss the rationale for using guinea pigs for this work. We then review guinea pig studies providing evidence for inflammatory mechanisms mediating both depressive-like behavior during separation as well as sensitization of stress responsiveness such as is thought to lead to increased vulnerability to depression at later ages. Finally, we discuss recent complementary work in adult monkeys that suggests cross-species generalizability of broad principles derived from the guinea pig experiments. Overall, the findings provide experimental support for human research implicating inflammatory mechanisms in the development of increased stress responsiveness and vulnerability to depression following attachment disruption and other forms of early-life stress. Specifically, the findings suggest inflammatory mechanisms may set in motion a cascade of underlying processes that mediate later increased stress responsiveness and, therefore, depression susceptibility.