长时间情绪和疼痛应激对神经系统对比兴奋性大鼠脑内bdnf基因表达的影响

I. Shalaginova, T. Zachepilo, N. Dyuzhikova
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摘要

背景:神经营养因子BDNF在神经元突触可塑性和功能活动中发挥重要作用,参与应激反应和应激后障碍的发病机制。由于神经系统兴奋性的遗传决定特征,应激后bdnf mRNA水平变化的特异性尚未研究。目的:研究正常状态和长时间情绪和痛苦应激暴露后(24小时、7、24、60天)不同时间神经系统兴奋性对比的两品系大鼠前额叶皮层、海马和杏仁核中bdnf mRNA的表达水平。材料与方法:选取两种不同神经系统兴奋性水平(HT高兴奋性阈值和LT低兴奋性阈值)的成年雄性大鼠进行研究。根据Hecht的说法,长期的情绪和痛苦暴露被用作慢性压力的模型。采用实时荧光定量PCR检测bdnf mRNA水平。研究两品系对照组和实验组大鼠在长时间情绪和疼痛应激后不同时间点(24小时、7天、24天、2个月)前额叶皮层、海马和杏仁核中bdnf mRNA水平的变化。结果:在高兴奋性LT大鼠中,暴露24小时后前额皮质bdnf基因表达下降,持续7天,暴露2个月后海马bdnf基因表达下降。在低兴奋性HT菌株大鼠中,未检测到bdnf mRNA的减少。结论:在高兴奋性LT大鼠中,长时间的情绪和疼痛应激可导致前额叶皮层和海马中bdnf基因的表达降低。在HT菌株的低兴奋大鼠中,在研究的任何脑区均未发现该神经营养因子mRNA水平的显著降低。与低兴奋大鼠相比,高兴奋大鼠应激后焦虑样行为障碍的严重程度可能与bdnf mRNA水平变化的特异性相关。
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The effect of prolonged emotional and pain stress on the expression of the bdnf gene in the brain of rats with contrast excitability of the nervous system
BACKGROUND: The neurotrophic factor BDNF performs important functions in synaptic plasticity and functional activity of neurons, involve in the stress response and the pathogenesis of post-stress disorders. The specificity of post-stress changes in the bdnf mRNA level due to genetically determined features of excitability of the nervous system has not been studied. AIM: To study the level of bdnf mRNA in the prefrontal cortex, hippocampus and amygdala of rats of two strains with contrasting excitability of the nervous system in normal condition and at different times after prolonged emotional and painful stress exposure (after 24 hours, 7, 24, 60 days). MATERIALS AND METHODS: The study was carried out on adult male rats of two strains with a different level of excitability of the nervous system (HT high threshold and LT low threshold of excitability). As a model of chronic stress, a long-term emotional and painful exposure according to Hecht was used. The bdnf mRNA level was determined using quantitative real-time PCR. Changes in the level of bdnf mRNA in the prefrontal cortex, hippocampus and amygdala of control and experimental groups of rats of two strains were studied at different time points (24 hours, 7, 24 days, 2 months) after prolonged emotional and painful stress exposure. RESULTS: It was found that in highly excitable LT rats, a decrease in the expression of the bdnf gene in the prefrontal cortex occurs 24 hours and persists up to 7 days after exposure, in the hippocampus 2 months after exposure. In rats of the low-excitable HT strain, the decrease in bdnf mRNA was not detected. CONCLUSIONS: In highly excitable LT rats, prolonged emotional and painful stress causes a decrease in the expression of the bdnf gene in the prefrontal cortex and hippocampus. In low-excitable rats of the HT strain, no significant decrease in the mRNA level of this neurotrophin was found in any of the studied brain regions. The possible association of this specificity of changes in the level of bdnf mRNA with a greater severity of post-stress anxiety-like behavior disorders in highly excitable rats compared with low-excitable ones is discussed.
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