Environmental enrichment attenuates depressive-like behavior in maternal rats by inhibiting neuroinflammation and apoptosis and promoting neuroplasticity
Guopeng Chen , Yuhui Zhang , Ruiling Li , Liuyin Jin , Keke Hao , Jingtong Rong , Hao Duan , Yiwei Du , Lihua Yao , Dan Xiang , Zhongchun Liu
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引用次数: 0
Abstract
Gestational stress can exacerbate postpartum depression (PPD), for which treatment options remain limited. Environmental enrichment (EE) may be a therapeutic intervention for neuropsychiatric disorders, including depression, but the specific mechanisms by which EE might impact PPD remain unknown. Here we examined the behavioral, molecular, and cellular impact of EE in a stable PPD model in rats developed through maternal separation (MS). Maternal rats subjected to MS developed depression-like behavior and cognitive dysfunction together with evidence of significant neuroinflammation including microglia activation, neuronal apoptosis, and impaired synaptic plasticity. Expanding the duration of EE to throughout pregnancy and lactation, we observed an EE-associated reversal of MS-induced depressive phenotypes, inhibition of neuroinflammation and neuronal apoptosis, and improvement in synaptic plasticity in maternal rats. Thus, EE effectively alleviates neuroinflammation, neuronal apoptosis, damage to synaptic plasticity, and consequent depression-like behavior in mother rats experiencing MS-induced PPD, paving the way for new preventive and therapeutic strategies for PPD.
妊娠压力会加重产后抑郁症(PPD),但治疗方法仍然有限。环境富集(EE)可能是治疗包括抑郁症在内的神经精神疾病的一种干预措施,但环境富集可能影响产后抑郁症的具体机制仍不清楚。在这里,我们研究了在通过母鼠分离(MS)建立的稳定 PPD 模型中,EE 对行为、分子和细胞的影响。接受 MS 的母体大鼠会出现抑郁样行为和认知功能障碍,并伴有明显的神经炎症,包括小胶质细胞活化、神经元凋亡和突触可塑性受损。将 EE 的持续时间延长至整个孕期和哺乳期,我们观察到 EE 可逆转 MS 诱导的抑郁表型,抑制神经炎症和神经元凋亡,并改善母体大鼠的突触可塑性。因此,EE能有效缓解神经炎症、神经元凋亡、突触可塑性损伤以及MS诱导的母鼠抑郁样行为,为PPD的预防和治疗新策略铺平道路。
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.