Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices.
Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices.
复制标题
短暂的恐惧导致杏仁核切片中去甲肾上腺素和 GABA 的诱发释放发生变化。
DOI：
10.1016/j.brainres.2007.01.038
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发表时间：
2007
期刊：
影响因子：
2.9
通讯作者：
Sanford,LarryD
中科院分区：
文献类型：
--
作者：
Liu,Xianling;Lonart,Gyorgy;Sanford,LarryD
先前与恐惧体验（电击脚）相关的音调提示的呈现产生了唤醒和睡眠的改变，这些改变发生在恐惧提示不再呈现之后。为了开始研究可能是恐惧线索呈现效应的神经化学机制，我们测量了已知调节唤醒状态和REM睡眠的大脑区域中[3 H]-去甲肾上腺素（[3 H]-NE]）和[14 C]-γ-氨基丁酸（[14 C]-GABA）的释放。将小鼠训练成能识别作为恐惧线索的音调，在暴露于恐惧线索后2-3 h，去极化诱发的小鼠杏仁核切片中[3 H]-NE的释放受到抑制，但在4-5 h后恢复。有趣的是，去极化诱发释放的[14 C]-GABA在杏仁核显着增加，也表现出增强的趋势，在海马，NPO，DRN在提示后2-3小时。[14 C]-GABA释放的变化也是短暂的;提示呈现后4-5小时，来自经历恐惧或中性提示的实验组的样品之间没有检测到显着差异。恐惧线索引起的神经递质释放变化与觉醒和REM睡眠变化的时间过程相似，这表明杏仁核神经传递的改变可能与恐惧后觉醒和睡眠的变化有关。
Presentation of a tonal cue that previously had been associated with a fearful experience (footshock) produces alterations in arousal and sleep that occur after the fearful cue is no longer presented. To begin investigating neurochemical mechanisms that may underlie the effects of fearful cue presentation, we measured release of [3H]-norepinephrine ([3H]-NE]) and [14C]-γ-amino-butyric acid ([14C]-GABA) from brain regions known to regulate arousal states and REM sleep. Depolarization-evoked release of [3H]-NE from amygdalar slices of mice, which were trained to recognize a tone as a fearful cue, was suppressed at 2–3 h after exposure of animals to the fearful cue, but recovered after 4–5 h. Interestingly, depolarization-evoked release of [14C]-GABA was significantly increased in the amygdala, and also showed a tendency for enhancement in the hippocampus, NPO, and DRN at 2–3 h after cue presentation. The changes in [14C]-GABA release were also transient; 4–5 h after cue presentation no significant differences were detected between samples derived from experimental groups which experienced fearful or neutral cues. The similar time course of fearful cue-induced changes in neurotransmitter release and changes in arousal and REM sleep suggests that alterations in amygdalar neurotransmission may be involved in the changes in arousal and sleep that occur after fear.