首页> 外文期刊>Acta neurobiologiae experimentalis >Effects of chronic forced swim stress on hippocampal brain-derived neutrophic factor (BDNF) and its receptor (TrkB) immunoreactive cells in juvenile and aged rats.
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Effects of chronic forced swim stress on hippocampal brain-derived neutrophic factor (BDNF) and its receptor (TrkB) immunoreactive cells in juvenile and aged rats.

机译:慢性强迫游泳应激对幼年和老年大鼠海马脑源性神经营养因子(BDNF)及其受体(TrkB)免疫反应性细胞的影响。

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摘要

A type of stress stimulation and age are claimed to affect the expression of brain-derived neurotrophic factor (BDNF) and its receptor - tyrosine kinase B (TrkB) in the hippocampal regions differentially. This study aimed to explore the influence of chronic (15 min daily for 21 days) forced swim stress (FS) exposure on the BDNF and TrkB containing neurons in the hippocampal CA1, CA3 pyramidal cell layers and dentate gyrus (DG) granule cell layer in juvenile (P28) and aged (P360) rats. An immunofluorescence (-ir) method was used to detect BDNF-ir and TrkB-ir cells. Under chronic FS exposure, in the group of juvenile rats a significant decrease in the density of BDNF immunoreactive neurons was observed in CA1 and DG (P less than <0.001), unlike CA3, where it remained unaltered just as the density of TrkB-ir cells in CA1 and DG, but in CA3 the number of TrkB-ir cells was found to grow (P less than 0.05) in comparison with control groups. After chronic FS exposure of aged (P360) rats, the density of BDNF-ir and TrkB-ir cells did not decline in any of the subregions of the hippocampus. In all subfields of the hippocampus, the denseness of BDNF-positive neurons was significantly higher in P360 stressed group, compared with P28 stressed group, but the density of TrkB-ir fell more markedly in P360 than in P28. In conclusion, chronic FS stress influenced the number of BDNF and TrkB immunoreactive neurons only in juvenile animals. The age of rats tested in the chronic forced swim test was a decisive factor determining changes in the density of BDNF-ir and TrkB-ir in the hippocampal structures.
机译:据称,一种压力刺激和年龄会影响海马区脑源性神经营养因子(BDNF)及其受体酪氨酸激酶B(TrkB)的表达。这项研究旨在探讨慢性(每天15分钟,每天21天)强迫游泳应激对BDNF和TrkB包含的海马CA1,CA3锥体细胞层和齿状回(DG)颗粒细胞层中神经元的影响。 (P28)和老年(P360)大鼠。免疫荧光(-ir)方法用于检测BDNF-ir和TrkB-ir细胞。在长期FS暴露下,在幼年大鼠组中,CA1和DG中的BDNF免疫反应性神经元密度显着下降(P小于<0.001),与CA3不同,CA3和TrkB-ir的密度保持不变。与对照组相比,CA1和DG中的TrkB-ir细胞数量增加(P小于0.05),但在CA3中TrkB-ir细胞的数量却增加了。在对老年(P360)大鼠进行长期FS暴露后,海马区的任何子区域BDNF-ir和TrkB-ir细胞的密度均未降低。在P360应激组中,海马的所有子区域中BDNF阳性神经元的密度均显着高于P28应激组,但是Prk中TrkB-ir的密度比P28下降得更为明显。总之,慢性FS应激仅影响幼年动物中BDNF和TrkB免疫反应性神经元的数量。在慢性强迫游泳试验中测试的大鼠年龄是决定海马结构中BDNF-ir和TrkB-ir密度变化的决定性因素。

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