Repeated exposure to antibiotics exhibits anxiety-like behaviors with a reduction in neurogenesis in the ventral hippocampus of dentate gyrus

IF 2 4区 医学 Q3 NEUROSCIENCES Neuroscience Letters Pub Date : 2025-02-16 Epub Date: 2025-01-20 DOI:10.1016/j.neulet.2025.138131
Kohei Takahashi , Kazuhiro Kurokawa , Kazuya Miyagawa , Atsumi Mochida-Saito , Hiroshi Takeda , Minoru Tsuji
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Abstract

Disruption of gut microbiota balance is known to contribute to the development of anxiety; however, it remains unclear whether dysbiosis-induced anxiety involves the glycogen synthase kinase-3β (GSK-3β)/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) pathway and neurogenesis in the ventral hippocampal dentate gyrus (DG). In this study, Male ddY mice were administered an antibacterial cocktail to induce dysbiosis. The dysbiosis model displayed anxiety-like behaviors in the hole-board and elevated plus-maze tests, decreased the phosphorylation levels of GSK-3β (Ser9) and CREB, decreased the expression level of BDNF in the ventral hippocampus, and reduced neurogenesis in the ventral hippocampal DG. This suggests that dysbiosis-induced anxiety-like behaviors are associated with reduced neurogenesis in the ventral hippocampal DG via the GSK-3β/CREB/BDNF pathway.
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反复暴露于抗生素表现出焦虑样行为,并减少齿状回腹侧海马的神经发生。
众所周知,肠道菌群平衡的破坏会导致焦虑的发展;然而,尚不清楚生态失调引起的焦虑是否涉及糖原合成酶激酶-3β (GSK-3β)/cAMP反应因子结合蛋白(CREB)/脑源性神经营养因子(BDNF)通路和海马腹侧齿状回(DG)的神经发生。在这项研究中,雄性小鼠被给予抗菌鸡尾酒诱导生态失调。生态失调模型在孔板和正迷宫实验中表现出焦虑样行为,降低GSK-3β (Ser9)和CREB的磷酸化水平,降低海马腹侧BDNF的表达水平,减少海马腹侧DG的神经发生。这表明生态失调诱导的焦虑样行为通过GSK-3β/CREB/BDNF通路与海马腹侧DG的神经发生减少有关。
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来源期刊
Neuroscience Letters
Neuroscience Letters 医学-神经科学
CiteScore
5.20
自引率
0.00%
发文量
408
审稿时长
50 days
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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