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A study of problems encountered in Granger causality analysis from a neuroscience perspective.从神经科学角度研究格兰杰因果分析中遇到的问题。
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Pica in Rats as a Preclinical Model of Emesis.大鼠异食癖作为呕吐的临床前模型
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Neural Correlates of Wakefulness, Sleep, and General Anesthesia: An Experimental Study in Rat.清醒、睡眠和全身麻醉的神经关联:大鼠实验研究
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High-frequency oscillations in human and monkey neocortex during the wake-sleep cycle.人类和猴子新皮层在觉醒-睡眠周期中的高频振荡。
Proc Natl Acad Sci U S A. 2016 Aug 16;113(33):9363-8. doi: 10.1073/pnas.1523583113. Epub 2016 Aug 1.
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Electroencephalogram signatures of ketamine anesthesia-induced unconsciousness.氯胺酮麻醉诱导意识丧失的脑电图特征。
Clin Neurophysiol. 2016 Jun;127(6):2414-22. doi: 10.1016/j.clinph.2016.03.005. Epub 2016 Mar 16.
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Thalamic reticular nucleus induces fast and local modulation of arousal state.丘脑网状核诱导觉醒状态的快速局部调节。
Elife. 2015 Oct 13;4:e08760. doi: 10.7554/eLife.08760.
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Age-dependent electroencephalogram (EEG) patterns during sevoflurane general anesthesia in infants.婴儿七氟醚全身麻醉期间的年龄依赖性脑电图(EEG)模式。
Elife. 2015 Jun 23;4:e06513. doi: 10.7554/eLife.06513.
8
Attenuation of high-frequency (50-200 Hz) thalamocortical EEG rhythms by propofol in rats is more pronounced for the thalamus than for the cortex.在大鼠中,丙泊酚对高频(50 - 200赫兹)丘脑皮质脑电图节律的衰减作用,对丘脑的影响比对皮质更明显。
PLoS One. 2015 Apr 15;10(4):e0123287. doi: 10.1371/journal.pone.0123287. eCollection 2015.
9
Disruption of thalamic functional connectivity is a neural correlate of dexmedetomidine-induced unconsciousness.丘脑功能连接的破坏是右美托咪定诱导昏迷的神经关联。
Elife. 2014 Nov 28;3:e04499. doi: 10.7554/eLife.04499.
10
Altered activity in the central medial thalamus precedes changes in the neocortex during transitions into both sleep and propofol anesthesia.在进入睡眠和丙泊酚麻醉状态的转变过程中,丘脑中央内侧核的活动改变先于新皮层的变化。
J Neurosci. 2014 Oct 1;34(40):13326-35. doi: 10.1523/JNEUROSCI.1519-14.2014.

丙泊酚诱导意识丧失及意识恢复过程中的丘脑-皮质同步性

Thalamocortical synchronization during induction and emergence from propofol-induced unconsciousness.

机构信息

Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114;

Harvard Medical School, Boston, MA 02115.

出版信息

Proc Natl Acad Sci U S A. 2017 Aug 8;114(32):E6660-E6668. doi: 10.1073/pnas.1700148114. Epub 2017 Jul 25.

DOI:10.1073/pnas.1700148114
PMID:28743752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5558998/
Abstract

General anesthesia (GA) is a reversible drug-induced state of altered arousal required for more than 60,000 surgical procedures each day in the United States alone. Sedation and unconsciousness under GA are associated with stereotyped electrophysiological oscillations that are thought to reflect profound disruptions of activity in neuronal circuits that mediate awareness and cognition. Computational models make specific predictions about the role of the cortex and thalamus in these oscillations. In this paper, we provide in vivo evidence in rats that alpha oscillations (10-15 Hz) induced by the commonly used anesthetic drug propofol are synchronized between the thalamus and the medial prefrontal cortex. We also show that at deep levels of unconsciousness where movement ceases, coherent thalamocortical delta oscillations (1-5 Hz) develop, distinct from concurrent slow oscillations (0.1-1 Hz). The structure of these oscillations in both cortex and thalamus closely parallel those observed in the human electroencephalogram during propofol-induced unconsciousness. During emergence from GA, this synchronized activity dissipates in a sequence different from that observed during loss of consciousness. A possible explanation is that recovery from anesthesia-induced unconsciousness follows a "boot-up" sequence actively driven by ascending arousal centers. The involvement of medial prefrontal cortex suggests that when these oscillations (alpha, delta, slow) are observed in humans, self-awareness and internal consciousness would be impaired if not abolished. These studies advance our understanding of anesthesia-induced unconsciousness and altered arousal and further establish principled neurophysiological markers of these states.

摘要

全身麻醉(GA)是一种药物诱导的意识改变状态,在美国每天就有超过 6 万例手术需要使用全身麻醉。GA 下的镇静和无意识与刻板的电生理振荡有关,这些振荡被认为反映了介导意识和认知的神经元回路中深刻的活动中断。计算模型对皮层和丘脑在这些振荡中的作用做出了具体的预测。在本文中,我们提供了大鼠体内的证据,表明常用麻醉药物异丙酚诱导的 alpha 振荡(10-15 Hz)在丘脑和内侧前额叶皮层之间是同步的。我们还表明,在运动停止的深度无意识状态下,会出现连贯的丘脑皮质 delta 振荡(1-5 Hz),与同时发生的慢振荡(0.1-1 Hz)不同。皮层和丘脑中的这些振荡结构与异丙酚诱导的无意识期间在人类脑电图中观察到的振荡结构非常相似。在全身麻醉苏醒期间,这种同步活动的消散顺序与意识丧失期间观察到的不同。一种可能的解释是,麻醉诱导的无意识的恢复遵循一个“启动”序列,由上升的觉醒中心主动驱动。内侧前额叶皮层的参与表明,如果没有消除的话,当这些振荡(alpha、delta、slow)在人类中被观察到时,自我意识和内部意识将会受到损害。这些研究增进了我们对麻醉诱导的无意识和觉醒改变的理解,并进一步确立了这些状态的神经生理学标记。