科研人员长久以来对于异丙酚等全身麻醉药物如何导致失去意识感到困惑，但是一项研究可能在大脑突然出现的一种电活动的模式中找到了一条线索，它可能与大脑不同区域之间信息传输被削弱有联系。
为了发现与失去意识有关的神经变化，Patrick Purdon及其同事测量了3名计划进行癫痫手术的病人在异丙酚诱导的麻醉期间的神经元和神经网络的电生理信号。随着这些病人进入无意识状态，这组作者观察到了称为慢振荡的信号的突然增加，这种信号与神经元在激活和非激活状态之间的交替有联系。作者发现，这些慢振荡在大脑皮层异步出现，这表明了不同的大脑区域在不同的时间激活。作者得出结论说，这种异步神经元活动预计会削弱皮层遥远区域之间的通信。
作者提出，慢振荡动态可能是异丙酚诱导产生的无意识的一个关键机制。作者说，这些发现可能帮助开发改良的麻醉监视系统和更安全的麻醉药物。（生物谷Bioon.com）
doi: 10.1073/pnas.1210907109
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Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness
Laura D. Lewis, Veronica S. Weiner, Eran A. Mukamel, Jacob A. Donoghue, Emad N. Eskandar, Joseph R. Madsen, William S. Anderson, Leigh R. Hochberg, Sydney S. Cash, Emery N. Brown, and Patrick L. Purdon
The neurophysiological mechanisms by which anesthetic drugs cause loss of consciousness are poorly understood. Anesthetic actions at the molecular, cellular, and systems levels have been studied in detail at steady states of deep general anesthesia. However, little is known about how anesthetics alter neural activity during the transition into unconsciousness. We recorded simultaneous multiscale neural activity from human cortex, including ensembles of single neurons, local field potentials, and intracranial electrocorticograms, during induction of general anesthesia. We analyzed local and global neuronal network changes that occurred simultaneously with loss of consciousness. We show that propofol-induced unconsciousness occurs within seconds of the abrupt onset of a slow (<1 Hz) oscillation in the local field potential. This oscillation marks a state in which cortical neurons maintain local patterns of network activity, but this activity is fragmented across both time and space. Local (<4 mm) neuronal populations maintain the millisecond-scale connectivity patterns observed in the awake state, and spike rates fluctuate and can reach baseline levels. However, neuronal spiking occurs only within a limited slow oscillation-phase window and is silent otherwise, fragmenting the time course of neural activity. Unexpectedly, we found that these slow oscillations occur asynchronously across cortex, disrupting functional connectivity between cortical areas. We conclude that the onset of slow oscillations is a neural correlate of propofol-induced loss of consciousness, marking a shift to cortical dynamics in which local neuronal networks remain intact but become functionally isolated in time and space.
