Erratum: Reduced Hippocampal Dendrite Branching, Spine Density and Neurocognitive Function in Premature Rabbits, and Reversal with Estrogen or TrkB Agonist Treatment
Erratum: Reduced Hippocampal Dendrite Branching, Spine Density and Neurocognitive Function in Premature Rabbits, and Reversal with Estrogen or TrkB Agonist Treatment
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勘误表：早产兔海马树突分支、脊柱密度和神经认知功能减少，以及雌激素或 TrkB 激动剂治疗的逆转
DOI：
10.1093/cercor/bhz155
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发表时间：
2019
期刊：
影响因子：
3.7
通讯作者：
Dobrenis, Kostantin
中科院分区：
文献类型：
--
作者：
Klebe, Damon;Tibrewal, Mahima;Sharma, Deep R;Vanaparthy, Rachna;Krishna, Sunil;Varghese, Merina;Cheng, Bokun;Mouton, Peter R;Velíšková, Jana;Dobrenis, Kostantin
早产儿患有神经和行为障碍。在此，我们假设早产和早产儿的非母体护理可能会破坏神经行为功能，海马树突分支和树突棘密度。此外，我们评估了17β-雌二醇（E2）替代或TrkB受体激动剂7，8-二羟基黄酮（DHF）是否会逆转早产新生儿受损的树突发育和认知功能。通过比较由实验室人员护理和灌胃喂养的早产（E28.5）兔套件与由其母兔在相同的孕后年龄饲养和母乳喂养的足月兔套件，对这些假设进行了检验。神经行为测试表明，早产和配方奶粉喂养与非产妇护理导致焦虑行为增加，社会互动差，缺乏新奇的偏好相比，术语包。树突状分支和总或蘑菇树突棘的数量减少，在CA 1领域的preterm套件与长期控制相比。尽管与足月对照组相比，早产儿试剂盒中的CDC 42和Rac 1/2/3表达水平较低，但RhoA活性较高。E2和DHF治疗逆转了早产引起的脊柱密度降低，降低了总RhoA-GTdR水平，并增强了认知功能。因此，早产儿和非产妇护理导致认知缺陷，并减少树突状乔木和棘在CA 1。E2替代或DHF治疗可能逆转树突棘的变化，改善早产儿的神经发育。
Preterm-born children suffer from neurological and behavioral disorders. Herein, we hypothesized that premature birth and non-maternal care of preterm newborns might disrupt neurobehavioral function, hippocampal dendritic arborization, and dendritic spine density. Additionally, we assessed whether 17β-estradiol (E2) replacement or the TrkB receptor agonist, 7,8-dihydroxyflavone (DHF), would reverse compromised dendritic development and cognitive function in preterm newborns. These hypotheses were tested by comparing preterm (E28.5) rabbit kits cared and gavage-fed by laboratory personnel and term-kits reared and breast-fed by their mother doe at an equivalent postconceptional age. Neurobehavioral tests showed that both premature-birth and formula-feeding with non-maternal care led to increased anxiety behavior, poor social interaction, and lack of novelty preference compared with term-kits. Dendritic branching and number of total or mushroom dendritic spines were reduced in the CA1 field of preterm-kits compared with term controls. While CDC42 and Rac1/2/3 expression levels were lower, RhoA-activity was higher in preterm-kits compared with term controls. Both E2 and DHF treatment reversed prematurity-induced reduction in spine density, reduced total RhoA-GTPase levels, and enhanced cognitive function. Hence, prematurity and non-maternal care result in cognitive deficits, and reduced dendritic arbors and spines in CA1. E2 replacement or DHF treatment might reverse changes in dendritic spines and improve neurodevelopment in premature infants.