The Impact of Cortical Deafferentation on the Neocortical Slow Oscillation
The Impact of Cortical Deafferentation on the Neocortical Slow Oscillation
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DOI：
10.1523/jneurosci.1156-13.2014
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发表时间：
2014-04-16
影响因子：
5.3
通讯作者：
Timofeev, Igor
中科院分区：
文献类型：
--
作者：
Lemieux, Maxime;Chen, Jen-Yung;Timofeev, Igor
慢振荡是哺乳动物深度睡眠时观察到的主要脑节律。虽然一些研究已经证明了它的新皮层起源，但丘脑的贡献程度仍然是一个讨论的问题。利用猫的体内电生理记录和计算模型，我们发现局部丘脑失活或完全隔离大脑内维持的新皮质板显著减少了受影响皮质区域的慢振荡和快速振荡的表达。慢振荡在丘脑失活12 h后开始恢复。缓慢的振荡，但不是更快的活动，在30小时后几乎恢复，并持续数周。我们还观察到，在丘脑失活几个小时后，体内记录的膜电位波动有所增加。在网络计算模型中模拟这种增强，增加长时间皮质内传入的突触后活动或缩放K（+）漏电流，但其他几种Na（+）和K（+）固有电流不足以恢复缓慢振荡。我们得出的结论是，在完整的大脑中，丘脑有助于产生皮层慢振荡的活跃状态，并介导其大规模同步。我们的研究还表明，大脑皮层内代偿机制可以抵消由去传入信号引起的睡眠慢振荡的改变，并且睡眠慢振荡是大脑新皮层的一种基本的内在状态。
Slow oscillation is the main brain rhythm observed during deep sleep in mammals. Although several studies have demonstrated its neocortical origin, the extent of the thalamic contribution is still a matter of discussion. Using electrophysiological recordings in vivo on cats and computational modeling, we found that the local thalamic inactivation or the complete isolation of the neocortical slabs maintained within the brain dramatically reduced the expression of slow and fast oscillations in affected cortical areas. The slow oscillation began to recover 12 h after thalamic inactivation. The slow oscillation, but not faster activities, nearly recovered after 30 h and persisted for weeks in the isolated slabs. We also observed an increase of the membrane potential fluctuations recorded in vivo several hours after thalamic inactivation. Mimicking this enhancement in a network computational model with an increased postsynaptic activity of long-range intracortical afferents or scaling K (+) leak current, but not several other Na (+) and K (+) intrinsic currents was sufficient for recovering the slow oscillation. We conclude that, in the intact brain, the thalamus contributes to the generation of cortical active states of the slow oscillation and mediates its large-scale synchronization. Our study also suggests that the deafferentation-induced alterations of the sleep slow oscillation can be counteracted by compensatory intracortical mechanisms and that the sleep slow oscillation is a fundamental and intrinsic state of the neocortex.