科研人員長久以來對(duì)于異丙酚等全身麻醉藥物如何導(dǎo)致失去意識(shí)感到困惑,，但是一項(xiàng)研究可能在大腦突然出現(xiàn)的一種電活動(dòng)的模式中找到了一條線索，它可能與大腦不同區(qū)域之間信息傳輸被削弱有聯(lián)系,。
為了發(fā)現(xiàn)與失去意識(shí)有關(guān)的神經(jīng)變化，Patrick Purdon及其同事測量了3名計(jì)劃進(jìn)行癲癇手術(shù)的病人在異丙酚誘導(dǎo)的麻醉期間的神經(jīng)元和神經(jīng)網(wǎng)絡(luò)的電生理信號(hào),。隨著這些病人進(jìn)入無意識(shí)狀態(tài),，這組作者觀察到了稱為慢振蕩的信號(hào)的突然增加，這種信號(hào)與神經(jīng)元在激活和非激活狀態(tài)之間的交替有聯(lián)系,。作者發(fā)現(xiàn),，這些慢振蕩在大腦皮層異步出現(xiàn)，這表明了不同的大腦區(qū)域在不同的時(shí)間激活,。作者得出結(jié)論說,，這種異步神經(jīng)元活動(dòng)預(yù)計(jì)會(huì)削弱皮層遙遠(yuǎn)區(qū)域之間的通信。
作者提出,，慢振蕩動(dòng)態(tài)可能是異丙酚誘導(dǎo)產(chǎn)生的無意識(shí)的一個(gè)關(guān)鍵機(jī)制,。作者說，這些發(fā)現(xiàn)可能幫助開發(fā)改良的麻醉監(jiān)視系統(tǒng)和更安全的麻醉藥物,。（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.
