Early life trauma increases threat response of peri-weaning rats, reduction of axo-somatic synapses formed by parvalbumin cells and perineuronal net in the basolateral nucleus of amygdala.
Early life trauma increases threat response of peri-weaning rats, reduction of axo-somatic synapses formed by parvalbumin cells and perineuronal net in the basolateral nucleus of amygdala.
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DOI：
10.1002/cne.24522
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发表时间：
2018-11-01
期刊：
影响因子：
--
通讯作者：
Aoki C
中科院分区：
文献类型：
--
作者：
Santiago AN;Lim KY;Opendak M;Sullivan RM;Aoki C
早期生活创伤是与情绪处理相关的终身障碍的风险因素，但其持久影响的知识尚不完整。这项研究的动机是这样的假设：早期生活创伤通过减少小白蛋白（PV）中间神经元和支持PV细胞的神经周围网（PNN）的抑制，从而增加杏仁核基底外侧（BLA）的兴奋性，从而增加杏仁核依赖的威胁反应。从出生日（PN） 8-12开始，将雌雄大鼠幼鼠饲养在正常垫料或不充足的筑巢材料下，以诱导母幼虐待创伤（稀缺-逆境模型，SAM）。在PN23断奶时，SAM组对捕食者气味的威胁反应增加。在正常饲养的PN22-23大鼠中，通过PN19-20的软骨素酶- abc和透明质酸酶单侧消耗BLA中的PNN，重现了sam诱导的威胁反应增加。光镜和电镜分析显示，SAM组的前-中水平BLA表现出PNN强度降低，pv -主锥体样神经元和pv - pv之间的轴-体突触减少。对照组（CON）和SAM组BLA中PV和PNN密度（细胞/ mm2）在PN12时仍较低，SAM延缓了PV强度和PNN密度的个体发生上升。此外，CON动物BLA前部至中部的PV细胞密度与威胁反应呈负相关，而SAM动物则无相关。因此，pnn支持的pv介导的锥体细胞体抑制的减少为早期生活虐待的持久影响提供了机制支持，表现为断奶时先天威胁反应的增加。
Early life trauma is a risk factor for life-long disorders related to emotional processing, but knowledge underlying its enduring effect is incomplete. This study was motivated by the hypothesis that early life trauma increases amygdala-dependent threat responses via reduction in inhibition by parvalbumin (PV) interneurons and perineuronal nets (PNN) supporting PV cells, thus increasing excitability of the basolateral amygdala (BLA). From postnatal day (PN) 8–12, rat pups of both sexes were reared under normal bedding or under insufficient nest-building materials to induce maternal-to-infant maltreatment trauma (Scarcity-Adversity Model, SAM). At weaning age of PN23, the SAM group exhibited increased threat responses to predator odor. The SAM-induced increase in threat response was recapitulated in normally reared PN22–23 rats that were unilaterally depleted of PNN in the BLA by the enzymes, chondroitinase-ABC plus hyaluronidase at PN19–20. Light and electron microscopic analysis of the BLA revealed that anterior-to-mid levels of SAM group’s BLAs exhibited decreased PNN intensity and decreased axo-somatic synapses between PV-to-principal pyramidal-like neurons and PV-to-PV. PV and PNN densities (cells/ mm2) in the BLA of both control (CON) and SAM groups were still low at PN12 and SAM delayed the ontogenetic rise of PV intensity and PNN density. Moreover, PV cell density in the anterior-to-mid BLA correlated negatively with threat response of CON animals, but not for SAM animals. Thus, reduction of PNN-supported, PV-mediated somatic inhibition of pyramidal cells provides a mechanistic support for the enduring effect of early life maltreatment manifested as increasing innate threat response at weaning.
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影响因子：
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