支持母性攻击性上升和下降的神经机制，这一成果由纽约大学林大宇团队经过不懈努力而取得。这一研究成果发表在2026年4月15日出版的国际学术期刊《自然》上。

母亲的攻击性使哺乳期的雌性能够保护它们脆弱的幼崽，但人们对其在出生后的迅速出现和在幼崽缺席时的迅速消退仍然知之甚少。他们的研究揭示了从表达雌激素受体α (PA^Esr1)的后杏仁核细胞到表达神经肽Y受体2 （VMHvl^Npy2r）的腹内侧下丘脑细胞的腹外侧部分的通路在母体攻击性的上升和下降中的关键作用。投射特异性操作和记录表明，PAEsr1细胞投射到VMHvl在攻击期间自然活跃，并且是母体攻击所必需的。

在哺乳期，PA-to-VMHvl^Npy2r突触增强，VMHvl^Npy2r细胞兴奋性增加，使攻击性增强。PA^Esr1神经元表达丰富的催产素受体，使催产素促进PA输出；幼崽移除后，催产素水平的下降降低了PA驱动并抑制了母性攻击，这一缺陷通过幼崽团聚或光遗传催产素的升高而恢复。这些发现揭示了PA^Esr1-VMHvl^Npy2r回路中多种形式的可塑性，这些可塑性共同实现了对母性攻击的适应性、基于需求的控制。

附：英文原文

Title: The neural mechanisms supporting the rise and fall of maternal aggression

Author: Yamaguchi, Takashi, Yan, Rongzhen, Khan, Mashrur, Kuno, Sota, Tewatia, Kanishk, Osakada, Takuya, Parthasarathy, Srinivas, Pacold, Michael E., Shah, Nirao M., Lin, Dayu

Issue&Volume: 2026-04-15

Abstract: Maternal aggression enables lactating females to protect their vulnerable young1,2, yet its rapid emergence after birth and swift decline when pups are absent remain poorly understood. Our study reveals the critical role of the pathway from posterior amygdala cells expressing oestrogen receptor alpha (PAEsr1) to the ventrolateral part of ventromedial hypothalamus cells expressing neuropeptide Y receptor 2 (VMHvlNpy2r) in the rise and fall of maternal aggression. Projection-specific manipulations and recordings show that PAEsr1 cells projecting to the VMHvl are naturally active during attack and are required for maternal aggression. During lactation, PA-to-VMHvlNpy2r synapses potentiate and VMHvlNpy2r cell excitability increases, enabling heightened aggression. PAEsr1 neurons express abundant oxytocin receptors, allowing oxytocin to boost PA output; after pup removal, declining oxytocin levels reduce PA drive and dampen maternal aggression, a deficit restored by pup reunion or optogenetic elevation of oxytocin. These findings reveal multiple forms of plasticity in a defined PAEsr1–VMHvlNpy2r circuit that collectively implement the adaptive, need-based control of maternal aggression.

DOI: 10.1038/s41586-026-10354-5

Source: https://www.nature.com/articles/s41586-026-10354-5