Department of Anesthesiology and Perioperative Care, University of California, Irvine, Irvine, California, USA.
Anesthesiology. 2012 Nov;117(5):981-95. doi: 10.1097/ALN.0b013e31826be467.
Work suggests the amnesia from dexmedetomidine (an α2-adrenergic agonist) is caused by a failure of information to be encoded into long-term memory and that dexmedetomidine might differentially affect memory for emotionally arousing material. We investigated these issues in humans using event-related neuroimaging to reveal alterations in brain activity and subsequent memory effects associated with drug exposure.
Forty-eight healthy volunteers received a computer-controlled infusion of either placebo or low-dose dexmedetomidine (target = 0.15 ng/ml plasma) during neuroimaging while they viewed and rated 80 emotionally arousing (e.g., graphic war wound) and 80 nonarousing neutral (e.g., cup) pictures for emotional arousal content. Long-term picture memory was tested 4 days later without neuroimaging. Imaging data were analyzed for drug effects, emotional processing differences, and memory-related changes with statistical parametric mapping-8.
Dexmedetomidine impaired overall (mean ± SEM) picture memory (placebo: 0.58 ± 0.03 vs. dexmedetomidine: 0.45 ± 0.03, P = 0.001), but did not differentially modulate memory as a function of item arousal. Arousing pictures were better remembered for both groups. Dexmedetomidine had regionally heterogeneous effects on brain activity, primarily decreasing it in the cortex and increasing it in thalamic and posterior hippocampal regions. Nevertheless, a single subsequent memory effect for item memory common to both groups was identified only in the left hippocampus/amygdala. Much of this effect was found to be larger for the placebo than dexmedetomidine group.
Dexmedetomidine impaired long-term picture memory, but did not disproportionately block memory for emotionally arousing items. The memory impairment on dexmedetomidine corresponds with a weakened hippocampal subsequent memory effect.
研究表明,右美托咪定(一种 α2-肾上腺素能激动剂)引起的遗忘是由于信息未能编码到长期记忆中,并且右美托咪定可能会对情绪激动的材料的记忆产生不同的影响。我们使用事件相关的神经影像学来研究这些问题,以揭示与药物暴露相关的大脑活动和随后的记忆效应的变化。
48 名健康志愿者在神经影像学检查期间接受了计算机控制的安慰剂或低剂量右美托咪定(目标 = 0.15ng/ml 血浆)输注,同时观看并对 80 张情绪激动(例如,图形战伤)和 80 张非情绪激动的中性(例如,杯子)图片进行情绪激动内容的评分。4 天后,在没有神经影像学检查的情况下测试长期图片记忆。使用统计参数映射-8 对成像数据进行分析,以评估药物作用、情绪处理差异以及与记忆相关的变化。
右美托咪定损害了整体(平均值±SEM)图片记忆(安慰剂:0.58±0.03 与右美托咪定:0.45±0.03,P=0.001),但不会根据项目唤醒程度调节记忆。两组都对唤醒图片的记忆更好。右美托咪定对大脑活动的影响具有区域异质性,主要是减少皮质中的活动,增加丘脑和后海马区域的活动。然而,仅在左侧海马/杏仁核中识别出了一个对两组项目记忆都有后续记忆效应的单一效应。该效应的大部分发现对于安慰剂组比右美托咪定组更大。
右美托咪定损害了长期图片记忆,但不会不成比例地阻止对情绪激动项目的记忆。在右美托咪定上的记忆损伤与海马体后续记忆效应减弱相对应。