Department of Psychology and The Gonda Brain Research Center, Bar-Ilan University, Ramat-Gan, Israel.
Functional Brain Center, Wohl Institute of Advanced Imaging, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
Neuropsychopharmacology. 2017 Nov;42(12):2301-2313. doi: 10.1038/npp.2017.71. Epub 2017 Apr 2.
Alloparental care, the cooperative care of offspring by group members other than the biological mother, has been widely practiced since early hominin evolution to increase infant survival and thriving. The coparental bond-a relationship of solidarity and commitment between two adults who join their effort to care for children-is a central contributor to children's well-being and sociality; yet, the neural basis of coparenting has not been studied in humans. Here, we followed 84 first-time co-parents (42 couples) across the first 6 years of family formation, including opposite-sex and same-sex couples, measured brain response to coparental stimuli, observed collaborative and undermining coparental behaviors in infancy and preschool, assayed oxytocin (OT) and vasopressin (AVP), and measured coparenting and child behavior problems at 6 years. Across family types, coparental stimuli activated the striatum, specifically the ventral striatum and caudate, striatal nodes implicated in motivational goal-directed social behavior. Psychophysiological interaction analysis indicated that both nodes were functionally coupled with the vmPFC in support of the human coparental bond and this connectivity was stronger as collaborative coparental behavior increased. Furthermore, caudate functional connectivity patterns differentiated distinct corticostriatal pathways associated with two stable coparental behavioral styles; stronger caudate-vmPFC connectivity was associated with more collaborative coparenting and was linked to OT, whereas a stronger caudate-dACC connectivity was associated with increase in undermining coparenting and was related to AVP. Finally, dyadic path-analysis model indicated that the parental caudate-vmPFC connectivity in infancy predicted lower child externalizing symptoms at 6 years as mediated by collaborative coparenting in preschool. Findings indicate that the coparental bond is underpinned by striatal activations and corticostriatal connectivity similar to other human affiliative bonds; highlight specific corticostriatal pathways as defining distinct coparental orientations that underpin family life; chart brain-hormone-behavior constellations for the mature, child-orientated coparental bond; and demonstrate the flexibility of this bond across family constellations and its unique contribution to child well-being.
亲代抚育,即除亲生母亲之外的群体成员对后代进行的合作式抚育,自早期人类进化以来就已广泛存在,其目的是提高后代的存活率和成长质量。共同抚育关系——两个成年人之间一种团结和承诺的关系,他们共同努力照顾孩子——是儿童福祉和社会性的核心贡献者;然而,人类共同抚育的神经基础尚未得到研究。在这里,我们跟踪了 84 对首次成为父母的人(42 对夫妇),跨越了家庭形成的前 6 年,包括异性恋和同性恋夫妇,测量了他们对共同抚育刺激的大脑反应,观察了婴儿期和幼儿期的合作和破坏共同抚育行为,检测了催产素(OT)和血管加压素(AVP),并在 6 岁时测量了共同抚育和儿童行为问题。在各种家庭类型中,共同抚育刺激激活了纹状体,特别是腹侧纹状体和尾状核,这些纹状体节点与动机导向的社交行为有关。心理生理交互分析表明,这两个节点与 vmPFC 都具有功能连接,以支持人类的共同抚育关系,并且这种连接随着合作性共同抚育行为的增加而增强。此外,尾状核的功能连接模式区分了与两种稳定的共同抚育行为方式相关的不同皮质纹状体通路;尾状核与 vmPFC 的连接越强,共同抚育行为越强,与 OT 有关,而尾状核与 dACC 的连接越强,与破坏共同抚育行为的增加有关,与 AVP 有关。最后,双路径分析模型表明,婴儿期父母尾状核与 vmPFC 的连接预测了 6 岁时儿童的外化症状较低,这是通过幼儿期的合作性共同抚育来介导的。研究结果表明,共同抚育关系是由纹状体激活和皮质纹状体连接支持的,类似于其他人类亲和关系;突出了特定的皮质纹状体通路作为定义不同的共同抚育取向的基础,这些取向支撑着家庭生活;为成熟的、以儿童为中心的共同抚育关系描绘了脑-激素-行为组合;并证明了这种关系在家庭结构中的灵活性及其对儿童福祉的独特贡献。