Adolescent stress impairs postpartum social behavior via anterior insula-prelimbic pathway in mice.
Adolescent stress impairs postpartum social behavior via anterior insula-prelimbic pathway in mice.
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DOI：
10.1038/s41467-023-38799-6
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发表时间：
2023-05-23
影响因子：
16.6
通讯作者：
Niwa, Minae
中科院分区：
文献类型：
--
作者：
Kin, Kyohei;Francis-Oliveira, Jose;Kano, Shin-ichi;Niwa, Minae
青春期压力可能是产后异常社会行为的危险因素，这严重影响个人的社会功能。尽管如此，潜在的机制仍不清楚。利用光遗传学和体内钙成像的小鼠模型，我们发现青春期心理社会应激，结合妊娠和分娩，导致从前脑岛到初级皮质的谷氨酸能通路(AI-PRL通路)功能低下，从而改变PRL神经元的活性，进而导致异常的社会行为。具体地说，AI-PRL途径通过调节PRL中的“稳定神经元”在识别其他小鼠的新颖性方面发挥了关键作用，这些神经元不断地被新小鼠激活或抑制。我们还观察到，AI-PRL途径中的糖皮质激素受体信号在应激诱导的产后变化中具有因果作用。我们的发现为青春期应激诱导的产后社会行为缺陷背后的皮质-皮质通路提供了功能洞察。青春期压力如何导致产后异常社会行为的机制尚不清楚。在这里，作者展示了一个潜在的机制，在小鼠中由前岛-初级皮质通路和糖皮质激素受体信号介导。
Adolescent stress can be a risk factor for abnormal social behavior in the postpartum period, which critically affects an individual social functioning. Nonetheless, the underlying mechanisms remain unclear. Using a mouse model with optogenetics and in vivo calcium imaging, we found that adolescent psychosocial stress, combined with pregnancy and delivery, caused hypofunction of the glutamatergic pathway from the anterior insula to prelimbic cortex (AI-PrL pathway), which altered PrL neuronal activity, and in turn led to abnormal social behavior. Specifically, the AI-PrL pathway played a crucial role during recognizing the novelty of other mice by modulating “stable neurons” in PrL, which were constantly activated or inhibited by novel mice. We also observed that glucocorticoid receptor signaling in the AI-PrL pathway had a causal role in stress-induced postpartum changes. Our findings provide functional insights into a cortico-cortical pathway underlying adolescent stress-induced postpartum social behavioral deficits. The mechanisms of how adolescent stress causes abnormal postpartum social behavior are unclear. Here, authors show an underlying mechanism mediating by the anterior insula-prelimbic cortex pathway and glucocorticoid receptor signaling in mice.
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