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模拟捕食者刺激会减少两种电鱼(物种名1和物种名2)的脑细胞增殖。

Simulated predator stimuli reduce brain cell proliferation in two electric fish species, and .

作者信息

Dunlap Kent D, Keane Geoffrey, Ragazzi Michael, Lasky Elise, Salazar Vielka L

机构信息

Department of Biology, Trinity College, Hartford, CT 06106, USA

Department of Biology, Trinity College, Hartford, CT 06106, USA.

出版信息

J Exp Biol. 2017 Jul 1;220(Pt 13):2328-2334. doi: 10.1242/jeb.158246.

DOI:10.1242/jeb.158246
PMID:28679791
Abstract

The brain structure of many animals is influenced by their predators, but the cellular processes underlying this brain plasticity are not well understood. Previous studies showed that electric fish () naturally exposed to high predator () density and tail injury had reduced brain cell proliferation compared with individuals facing few predators and those with intact tails. However, these field studies described only correlations between predator exposure and cell proliferation. Here, we used a congener and another electric fish to experimentally test the hypothesis that exposure to a predator stimulus and tail injury causes alterations in brain cell proliferation. To simulate predator exposure, we either amputated the tail followed by short-term (1 day) or long-term (17-18 days) recovery or repeatedly chased intact fish with a plastic rod over a 7 day period. We measured cell proliferation (PCNA+ cell density) in the telencephalon and diencephalon, and plasma cortisol, which commonly mediates stress-induced changes in brain cell proliferation. In both species, either tail amputation or simulated predator chase decreased cell proliferation in the telencephalon in a manner resembling the effect of predators in the field. In , cell proliferation decreased drastically in the short term after tail amputation and partially rebounded after long-term recovery. In , tail amputation elevated cortisol levels, but repeated chasing had no effect. In , tail amputation elevated cortisol levels in the short term but not in the long term. Thus, predator stimuli can cause reductions in brain cell proliferation, but the role of cortisol is not clear.

摘要

许多动物的大脑结构会受到其捕食者的影响,但其大脑可塑性背后的细胞过程却尚未得到充分理解。先前的研究表明,与那些面临较少捕食者且尾巴完好无损的个体相比,自然暴露于高捕食者密度环境且尾巴受伤的电鱼,其脑细胞增殖有所减少。然而,这些实地研究仅描述了捕食者暴露与细胞增殖之间的相关性。在此,我们使用一种同属物种以及另一种电鱼进行实验,以检验以下假设:暴露于捕食者刺激和尾巴受伤会导致脑细胞增殖发生改变。为了模拟捕食者暴露,我们要么截断尾巴,然后让其短期(1天)或长期(17 - 18天)恢复,要么在7天时间里用塑料棒反复追逐完好无损的鱼。我们测量了端脑和间脑中的细胞增殖(增殖细胞核抗原阳性细胞密度)以及血浆皮质醇水平,血浆皮质醇通常介导应激诱导的脑细胞增殖变化。在这两个物种中,截断尾巴或模拟捕食者追逐都会使端脑中的细胞增殖减少,其方式类似于野外捕食者的影响。在某一物种中,截断尾巴后短期内细胞增殖急剧下降,长期恢复后部分反弹。在另一物种中,截断尾巴会提高皮质醇水平,但反复追逐则没有效果。在又一物种中,截断尾巴在短期内会提高皮质醇水平,但长期则不然。因此,捕食者刺激会导致脑细胞增殖减少,但皮质醇的作用尚不清楚。

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