哺乳動物后代如果在子宮中發(fā)育時缺乏某些荷爾蒙,，那么當(dāng)它們成年時就更有可能產(chǎn)生焦慮。在本期Nature Communications上報告的這些發(fā)現(xiàn)讓我們對胎盤在情緒行為的長期編程中所起作用有了新認(rèn)識。
“胰島素樣生長因子-2”曾被發(fā)現(xiàn)在哺乳動物的胎兒和胎盤發(fā)育中扮演一個主要角色,，而且這種荷爾蒙在胎盤和胎兒中的表達(dá)的變化也被發(fā)現(xiàn)與子宮中的生長限制有關(guān)。雖然子宮內(nèi)的生長限制已知影響新生兒的發(fā)育,，但其長期后果卻并不完全清楚,。Lawrence Wilkinson及其同事研究了僅在胎盤中缺少“胰島素樣生長因子-2”的小鼠的成年行為,，發(fā)現(xiàn)這些小鼠與焦慮有關(guān)的行為特征增加，同時伴隨著腦中與這種行為有關(guān)的基因表達(dá)的特定變化,。
雖然這些研究是用小鼠完成的,，但這些發(fā)現(xiàn)對人類發(fā)育可能會有更廣泛的意義。然而,，還需要進(jìn)一步的研究來確定這一猜測在多大程度上是正確的,。（生物谷 Bioon.com）
生物谷推薦的英文摘要
Nature Communications doi:10.1038/ncomms3311
Placental programming of anxiety in adulthood revealed by Igf2-null models
Mikael Allan Mikaelsson, Miguel Constância, Claire L. Dent, Lawrence S. Wilkinson & Trevor Humby
Imprinted, maternally silenced insulin-like growth factor-2 is expressed in both the foetus and placenta and has been shown to have roles in foetal and placental development in animal models. Here we compared mice engineered to be null for the placenta-specific P0 transcript (insulin-like growth factor-2-P0 KO) to mice with disruptions of all four insulin-like growth factor-2 transcripts, and therefore null for insulin-like growth factor-2 in both placenta and foetus (insulin-like growth factor-2-total KO). Both models lead to intrauterine growth restriction but dissociate between a situation where there is an imbalance between foetal demand and placental supply of nutrients (the insulin-like growth factor-2-P0 KO) and one where demand and supply is more balanced (the insulin-like growth factor-2-total KO). Increased reactivity to anxiety-provoking stimuli is manifested later in life only in those animals where there is a mismatch between placental supply and foetal demand for nutrients during gestation. Our findings further distinguish placental dysfunction from intrauterine growth restriction and reveal a role for the placenta in long-term programming of emotional behaviour.
