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大鼠急性足底电击应激后脑去甲肾上腺素的延迟增加。

Delayed increase of brain noradrenaline after acute footshock stress in rats.

机构信息

Stress Disorders Research Team, Tokyo Institute of Psychiatry, 2-1-8 Kamikitazawa, Setagaya-ku, Tokyo, 156-8585, Japan.

出版信息

Neurochem Res. 2010 Mar;35(3):412-7. doi: 10.1007/s11064-009-0070-1. Epub 2009 Oct 1.

DOI:10.1007/s11064-009-0070-1
PMID:19795208
Abstract

Several lines of evidence strongly suggest that accumulation of noradrenaline (NA) in the brain may underlie the hyperarousal symptoms experienced in post-traumatic stress disorder. In animal experiments, however, the effect of stress on NA content appears complex; acute stress reduces the level, while chronic stress tends to increase it. To explain this discrepancy, it is necessary to observe the long-term effects of acute stress on NA metabolism in the brain. In this study, rats were exposed to intermittent intense footshock stress for 1 h, and the brain NA content was measured for 7 days after the stress stimulus. Hypothalamic NA content was immediately reduced and recovered within 24 h. However, a significant NA increase was observed 7 days after the footshock. In the cerebral cortex and hippocampus, an increase in NA content was observed 1 day after the stress and lasted for at least 7 days. The fact that the content of 3-methoxy-4-hydroxyphenylglycol, a major NA metabolite, only transiently increased in all these regions possibly reflects NA release. These results indicate that increase in the brain NA content can be induced by acute stress, though its emergence is delayed. Importantly, this suggests that both acute and chronic stress may lead to NA accumulation under the same mechanism.

摘要

有几条证据强烈表明,大脑中去甲肾上腺素(NA)的积累可能是创伤后应激障碍中过度觉醒症状的基础。然而,在动物实验中,应激对 NA 含量的影响似乎很复杂;急性应激会降低其水平,而慢性应激则倾向于增加其水平。为了解释这种差异,有必要观察急性应激对大脑中 NA 代谢的长期影响。在这项研究中,大鼠接受了 1 小时的间歇性强烈足底电击应激,应激刺激后 7 天测量大脑 NA 含量。下丘脑 NA 含量立即减少,并在 24 小时内恢复。然而,在足底电击后 7 天观察到显著的 NA 增加。在大脑皮层和海马体中,应激后 1 天观察到 NA 含量增加,并持续至少 7 天。事实上,所有这些区域中 3-甲氧基-4-羟苯乙二醇(一种主要的 NA 代谢物)的含量仅短暂增加,可能反映了 NA 的释放。这些结果表明,急性应激可诱导大脑 NA 含量增加,尽管其出现是延迟的。重要的是,这表明急性和慢性应激可能通过相同的机制导致 NA 积累。

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STRESS-INDUCED RELEASE OF BRAIN NOREPINEPHRINE AND ITS INHIBITION BY DRUGS.应激诱导的脑去甲肾上腺素释放及其药物抑制作用。
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Neurotransmitter Systems in a Mild Blast Traumatic Brain Injury Model: Catecholamines and Serotonin.轻度爆炸创伤性脑损伤模型中的神经递质系统:儿茶酚胺和血清素。
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