Department of Anatomy and Neurobiology, Medical University of Gdańsk, Dębinki 1 St., 80–211 Gdańsk, Poland.
Brain Res. 2011 Apr 12;1384:97-109. doi: 10.1016/j.brainres.2011.01.112. Epub 2011 Mar 5.
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.
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。