Microglia are necessary for probiotics supplementation to improve impaired fear extinction caused by pregnancy stress in adult offspring of rats

IF 4.3 2区 医学 Q1 NEUROSCIENCES Neurobiology of Stress Pub Date : 2023-11-19 DOI:10.1016/j.ynstr.2023.100591
Ru Zeng , Jie Chen , Yihan Peng , Weiye Xu , Yuanyuan Tao , Min Li , Ruqi Zhang , Jingzhuo Meng , Zhiyuan Li , Leping Zeng , Jufang Huang
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Abstract

The prevention and treatment of fear-related disorders in offspring affected by pregnancy stress remains challenging at clinic. Here, we examined the effects of gut microbiota of stressed pregnant rats on the fear extinction of their offsprings, and the potential mechanisms. We found that gut microbiota transplantation from rats with pregnancy stress to normal pregnant rats impaired fear extinction, induced microglial activation and synaptic phagocytosis, increased synapse loss in offsprings. Probiotics supplement during pregnancy stress partly normalized pregnancy stress-induced gut microbiota dysbiosis of pregnant rats, and promoted fear memory extinction, inhibited fear memory reappearance, and limited microglial activation and synaptic phagocytosis in offsprings. These data revealed that gut microbiota of stressed pregnant mother improved the development of fear-related disorders of offspring, which may be associated with microglial synaptic pruning.

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小胶质细胞是补充益生菌改善大鼠成年后代妊娠应激引起的恐惧消退障碍所必需的
预防和治疗受妊娠压力影响的后代的恐惧相关障碍在临床上仍然具有挑战性。在这里,我们研究了应激怀孕大鼠肠道微生物群对其后代恐惧灭绝的影响及其潜在机制。我们发现,将妊娠应激大鼠的肠道菌群移植到正常妊娠大鼠的后代中,会损害恐惧消退,诱导小胶质细胞激活和突触吞噬,增加突触损失。妊娠应激期间补充益生菌可部分缓解妊娠应激引起的妊娠大鼠肠道菌群失调,促进后代恐惧记忆消退,抑制恐惧记忆重现,限制小胶质细胞激活和突触吞噬。这些数据表明,压力孕妇的肠道微生物群改善了后代恐惧相关疾病的发展,这可能与小胶质突触修剪有关。
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来源期刊
Neurobiology of Stress
Neurobiology of Stress Biochemistry, Genetics and Molecular Biology-Biochemistry
CiteScore
9.40
自引率
4.00%
发文量
74
审稿时长
48 days
期刊介绍: Neurobiology of Stress is a multidisciplinary journal for the publication of original research and review articles on basic, translational and clinical research into stress and related disorders. It will focus on the impact of stress on the brain from cellular to behavioral functions and stress-related neuropsychiatric disorders (such as depression, trauma and anxiety). The translation of basic research findings into real-world applications will be a key aim of the journal. Basic, translational and clinical research on the following topics as they relate to stress will be covered: Molecular substrates and cell signaling, Genetics and epigenetics, Stress circuitry, Structural and physiological plasticity, Developmental Aspects, Laboratory models of stress, Neuroinflammation and pathology, Memory and Cognition, Motivational Processes, Fear and Anxiety, Stress-related neuropsychiatric disorders (including depression, PTSD, substance abuse), Neuropsychopharmacology.
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