Rat strain differences in restraint stress-induced brain cytokines.
Rat strain differences in restraint stress-induced brain cytokines.
复制标题
约束应力诱导的脑细胞因子的大鼠菌株差异。
DOI：
10.1016/j.neuroscience.2011.05.023
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发表时间：
2011-08-11
期刊：
影响因子：
3.3
通讯作者：
Johnson, J. D.
中科院分区：
文献类型：
--
作者：
Porterfield, V. M.;Zimomra, Z. R.;Caldwell, E. A.;Camp, R. M.;Gabella, K. M.;Johnson, J. D.
在压力期间诱导脑细胞因子对改变行为、情绪和认知功能具有强有力的影响。目前，尚不清楚为什么暴露于某些应激源（如尾震和足震）会升高脑细胞因子，而暴露于游泳，捕食者气味和束缚应激则不会。最近的数据表明，脑去甲肾上腺素能信号介导脑细胞因子的产生，表明在应激过程中去甲肾上腺素释放的幅度可能是启动脑细胞因子产生的关键。本研究的目的是探讨应激诱导的脑细胞因子之间的大鼠品系，不同的应激反应的幅度，脑去甲肾上腺素和HPA反应。将Sprague-Dawley和Fischer大鼠置于束缚袋中1 h或2 h，并在应激终止后立即处死。束缚暴露后1h，高应激反应Fischer大鼠下丘脑IL-1β和IL-1 R2 mRNA水平显著升高，2 h后IL-1β蛋白水平显著升高，而Sprague-Dawley大鼠下丘脑IL-1β和IL-1 R2 mRNA水平无显著变化。IL-6、IL-1 R1、IL-1 RA和考克斯-2 mRNA没有改变，海马中任何细胞因子的表达或两种菌株中循环细胞因子的表达也没有改变。地昔帕明（一种去甲肾上腺素再摄取抑制剂）单独给药或与应激联合给药足以增加下丘脑中的IL-1β mRNA，地昔帕明与应激联合给药足以增加下丘脑中的IL-1 R2 mRNA。这些数据支持我们的假设，即有一个关键的阈值，脑去甲肾上腺素刺激脑细胞因子，这可能有助于解释为什么严重的压力更常见的报告，以诱导脑细胞因子。这些数据还表明，生物体对应激诱导的脑细胞因子产生的易感性取决于去甲肾上腺素能神经元的反应性和调节。
Induction of brain cytokines during times of stress has potent effects on altering behavior, mood, and cognitive functioning. Currently, it is unknown why exposure to some stressors such as tailshock and footshock elevate brain cytokines, while exposure to swim, predator odor, and restraint stress do not. Recent data indicate that brain noradrenergic signaling mediates brain cytokine production suggests magnitude of norepinephrine release during stress may be critical in initiating brain cytokine production. The aim of the current study was to investigate stress-induced brain cytokines between rat strains that differ in their magnitude of stress responsiveness as measured by brain norepinephrine and HPA responses. Sprague-Dawley and Fischer rats were placed in a restraint bag for 1h or 2h and sacrificed immediately following stressor termination. Exposure to restraint significantly elevated hypothalamic IL-1β and IL-1R2 mRNA after 1h and IL-1β protein after 2h in the high stress responsive Fischer rats, but not in Sprague-Dawley rats. IL-6, IL-1R1, Il-1RA and Cox-2 mRNA were not altered and neither was expression of any cytokines in the hippocampus or circulating cytokines in either strain. Administration of desipramine (a norepinephrine reuptake inhibitor) to Sprague-Dawley rats was sufficient either alone or in combination with stress to increase IL-1β mRNA in the hypothalamus and desipramine combined with stress was sufficient to increase IL-1R2 mRNA in the hypothalamus. These data support our hypothesis that there is a critical threshold of brain norepinephrine necessary to stimulate brain cytokines, which may help to explain why severe stressors are more commonly reported to induce brain cytokines. These data also suggest an organisms’ susceptibility to stress-induced brain cytokine production depends on responsiveness and regulation of noradrenergic neurons.
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