Kuroda Y, McEwen B S
Laboratory of Neuroendocrinology, Rockefeller University, New York, NY, USA.
Brain Res Mol Brain Res. 1998 Aug 15;59(1):35-9. doi: 10.1016/s0169-328x(98)00130-2.
Chronic restraint stress of rats for three weeks produces an atrophy of apical dendrites in the CA3 region of the hippocampus. This alteration is blocked by the novel antidepressant, tianeptine. In order to investigate the underlying mechanism of these phenomena, we evaluated the effect of chronic restraint and tianeptine on mRNA expression of neurotrophic factors such as brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and basic fibroblast growth factor (bFGF). Chronic restraint and tianeptine treatment did not change the expression of these neurotrophins in the rat hippocampus. We also evaluated the effects of stress and tianeptine on GAP-43 and MAP2, both of which are known to be related to the development of neurons. Chronic restraint resulted in a small decrease in GAP-43 mRNA expression in the CA3 region of the hippocampus, which was not prevented by the concomitant administration of tianeptine. MAP2 mRNA expression was not changed by either chronic stress or tianeptine treatment. We conclude that these neurotrophins, GAP-43 and MAP2 are not likely to be directly related to the chronic stress-induced dendritic atrophy or the prevention of the atrophy by tianeptine.
对大鼠进行为期三周的慢性束缚应激会导致海马体CA3区顶端树突萎缩。新型抗抑郁药噻奈普汀可阻止这种改变。为了探究这些现象的潜在机制，我们评估了慢性束缚和噻奈普汀对脑源性神经营养因子（BDNF）、神经营养因子-3（NT-3）和碱性成纤维细胞生长因子（bFGF）等神经营养因子mRNA表达的影响。慢性束缚和噻奈普汀处理并未改变大鼠海马体中这些神经营养因子的表达。我们还评估了应激和噻奈普汀对GAP-43和MAP2的影响，已知这两者都与神经元发育有关。慢性束缚导致海马体CA3区GAP-43 mRNA表达略有下降，同时给予噻奈普汀并不能阻止这种下降。慢性应激或噻奈普汀处理均未改变MAP2 mRNA表达。我们得出结论，这些神经营养因子、GAP-43和MAP2不太可能与慢性应激诱导的树突萎缩或噻奈普汀对萎缩的预防直接相关。
