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Exposure to bacterial lipopolysaccharide in early life affects the expression of ionotropic glutamate receptor genes and is accompanied by disturbances in long-term potentiation and cognitive functions in young rats
Brain, Behavior, and Immunity ( IF 15.1 ) Pub Date : 2020-11-01 , DOI: 10.1016/j.bbi.2020.07.034
Olga E Zubareva 1 , Tatyana Y Postnikova 2 , Alexandra V Grifluk 2 , Alexander P Schwarz 2 , Ilya V Smolensky 2 , Anton A Karepanov 2 , Dmitry S Vasilev 2 , Ekaterina A Veniaminova 3 , Alexander Y Rotov 2 , Sergey V Kalemenev 2 , Aleksey V Zaitsev 2
Affiliation  

Infections in childhood play an essential role in the pathogenesis of cognitive and psycho-emotional disorders. One of the possible mechanisms of these impairments is changes in the functional properties of NMDA and AMPA glutamate receptors in the brain. We suggest that bacterial infections during the early life period, which is critical for excitatory synapse maturation, can affect the subunit composition of NMDA and AMPA receptors. In the present study, we investigated the effect of repetitive lipopolysaccharide (LPS) intraperitoneal (i.p.) administration (25 μg/kg/day on P14, 16, and 18), mimicking an infectious disease, on the expression of subunits of NMDA and AMPA receptors in young rats. We revealed a substantial decrease of GluN2B subunit expression in the hippocampus at P23 using Western blot analysis and real-time polymerase chain reaction assay. Moderate changes were also found in GluN1, GluN2A, and GluA1 mRNA expression. The LPS-treated rats exhibited decreased exploratory and locomotor activity in the open field test and the impairment of spatial learning in the Morris water maze. Behavioral impairments were accompanied by a significant reduction in long-term hippocampal synaptic potentiation. Our data indicate that LPS-treatment in the critical period for excitatory synapse maturation alters ionotropic glutamate receptor gene expression, disturbs synaptic plasticity, and alters behavior.

中文翻译:

早年接触细菌脂多糖会影响离子型谷氨酸受体基因的表达,并伴有幼鼠长时程增强和认知功能障碍

儿童时期的感染在认知和心理情绪障碍的发病机制中起着至关重要的作用。这些损伤的可能机制之一是大脑中 NMDA 和 AMPA 谷氨酸受体的功能特性发生变化。我们认为生命早期的细菌感染对兴奋性突触成熟至关重要,可影响 NMDA 和 AMPA 受体的亚基组成。在本研究中,我们研究了重复性脂多糖 (LPS) 腹膜内 (ip) 给药(P14、16 和 18 日为 25 μg/kg/天)模拟传染病对 NMDA 和 AMPA 亚基表达的影响幼鼠中的受体。我们使用蛋白质印迹分析和实时聚合酶链反应测定揭示了 P23 海马中 GluN2B 亚基表达的显着降低。在 GluN1、GluN2A 和 GluA1 mRNA 表达中也发现了适度的变化。LPS 治疗的大鼠在野外试验中表现出探索性和自发性活动减少,以及在莫里斯水迷宫中空间学习受损。行为障碍伴随着长期海马突触增强的显着降低。我们的数据表明,在兴奋性突触成熟的关键时期,LPS 治疗会改变离子型谷氨酸受体基因表达,扰乱突触可塑性,并改变行为。LPS 治疗的大鼠在野外试验中表现出探索性和自发性活动减少,以及在莫里斯水迷宫中空间学习受损。行为障碍伴随着长期海马突触增强的显着降低。我们的数据表明,在兴奋性突触成熟的关键时期,LPS 治疗会改变离子型谷氨酸受体基因表达,扰乱突触可塑性,并改变行为。LPS 治疗的大鼠在野外试验中表现出探索性和自发性活动减少,以及在莫里斯水迷宫中空间学习受损。行为障碍伴随着长期海马突触增强的显着降低。我们的数据表明,在兴奋性突触成熟的关键时期,LPS 治疗会改变离子型谷氨酸受体基因表达,扰乱突触可塑性,并改变行为。
更新日期:2020-11-01
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