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两种急性和慢性应激刺激模型是否会影响中年大鼠海马神经元中神经生长因子(NGF)及其受体 TrkA 的含量?

Do two models of acute and chronic stress stimulation influence the amount of nerve growth factor (NGF) and its receptor TrkA in the hippocampal neurons of middle aged rats?

机构信息

Department of Anatomy and Neurobiology, Medical University of Gdańsk, Dębinki 1 St., 80–211 Gdańsk, Poland.

出版信息

Brain Res. 2011 Apr 12;1384:97-109. doi: 10.1016/j.brainres.2011.01.112. Epub 2011 Mar 5.

Abstract

Our study aimed to explore the influence of two different stressors: acute (once for 15 min) and chronic (15 min daily for 21 days) exposure to high light open field (HL-OF) or forced swim (FS) on the density of nerve growth factor (NGF) and tyrosine kinase A (TrkA) immunoreactive neurons in the hippocampal CA1 and CA3 pyramidal cell layers and dentate gyrus (DG) granule cell layer in middle aged (360 days old; P360; P, postnatal day) rats. In contrast to non-stressed animals, acute HL-OF stimulation resulted in an increase (p<0.001) in the density of NGF-ir cells in CA1, CA3, DG, whereas chronic HL-OF produced no changes in all hippocampal regions. The rats which underwent acute and chronic FS tests showed no statistically significant differences in the density of NGF-ir containing cells in the CA1, CA3, and DG subfields compared with control rats. Except for DG, where after 21 days of FS the density of TrkA-ir neurons was found to increase (p<0.05) in comparison to unstressed rats, no changes were noted in the density of TrkA-ir in the studied hippocampal structures as a result of acute and chronic HL-OF or FS exposure. These results indicate that acute HL-OF stress stimulation was the only factor inducing changes in the density of NGF-ir containing neurons in the hippocampal CA1, CA3, and DG of middle aged rats. In respect of the density of NGF-ir and TrkA-ir cells in the hippocampal structures, prolonged exposure to HL-OF or FS stressors did not constitute an aggravating factor for rats in the studied ontogenetic period.

摘要

我们的研究旨在探讨两种不同应激源的影响

急性(15 分钟一次)和慢性(15 分钟每天持续 21 天)暴露于高光开放场(HL-OF)或强迫游泳(FS)对中年(360 天龄;P360;P,出生后第)大鼠海马 CA1 和 CA3 锥体细胞层和齿状回(DG)颗粒细胞层中神经生长因子(NGF)和酪氨酸激酶 A(TrkA)免疫反应性神经元的密度。与未受应激的动物相比,急性 HL-OF 刺激导致 CA1、CA3、DG 中 NGF-ir 细胞密度增加(p<0.001),而慢性 HL-OF 则没有改变所有海马区。接受急性和慢性 FS 测试的大鼠在 CA1、CA3 和 DG 亚区中 NGF-ir 细胞的密度与对照组大鼠相比没有统计学上的显著差异。除 DG 外,经过 21 天 FS 后,DG 中 TrkA-ir 神经元的密度增加(p<0.05)与未受应激的大鼠相比,急性和慢性 HL-OF 或 FS 暴露后,研究中的海马结构中 TrkA-ir 神经元的密度没有变化。这些结果表明,急性 HL-OF 应激刺激是唯一导致中年大鼠海马 CA1、CA3 和 DG 中 NGF-ir 神经元密度发生变化的因素。在海马结构中 NGF-ir 和 TrkA-ir 细胞的密度方面,长时间暴露于 HL-OF 或 FS 应激源不会成为研究发育阶段大鼠的加重因素。

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