Breakdown of local information processing may underlie isoflurane anesthesia effects

The disruption of coupling between brain areas has been suggested as the mechanism underlying loss of consciousness in anesthesia. This hypothesis has been tested previously by measuring the information transfer between brain areas, and by taking reduced information transfer as a proxy for decoupling. Yet, information transfer is a function of the amount of information available in the information source—such that transfer decreases even for unchanged coupling when less source information is available. Therefore, we reconsidered past interpretations of reduced information transfer as a sign of decoupling, and asked whether impaired local information processing leads to a loss of information transfer. An important prediction of this alternative hypothesis is that changes in locally available information (signal entropy) should be at least as pronounced as changes in information transfer. We tested this prediction by recording local field potentials in two ferrets after administration of isoflurane in concentrations of 0.0%, 0.5%, and 1.0%. We found strong decreases in the source entropy under isoflurane in area V1 and the prefrontal cortex (PFC)—as predicted by our alternative hypothesis. The decrease in source entropy was stronger in PFC compared to V1. Information transfer between V1 and PFC was reduced bidirectionally, but with a stronger decrease from PFC to V1. This links the stronger decrease in information transfer to the stronger decrease in source entropy—suggesting reduced source entropy reduces information transfer. This conclusion fits the observation that the synaptic targets of isoflurane are located in local cortical circuits rather than on the synapses formed by interareal axonal projections. Thus, changes in information transfer under isoflurane seem to be a consequence of changes in local processing more than of decoupling between brain areas. We suggest that source entropy changes must be considered whenever interpreting changes in information transfer as decoupling.有研究提出，脑区间耦合破坏是全身麻醉下意识丧失的潜在机制。此前已有研究通过测量脑区间的信息传递，并以降低的信息传递作为解耦的替代指标，对该假说进行了验证。然而，信息传递是信息源可用信息量的函数——当源可用信息量减少时，即便脑区间耦合状态未发生改变，信息传递也会随之降低。因此，我们重新审视了此前将信息传递降低视为脑区解耦标志的解读，并提出核心疑问：局部信息处理功能受损是否会引发信息传递丧失？这一替代性假说的一项重要预测为，局部可用信息（信号熵，signal entropy）的变化幅度至少应与信息传递的变化幅度相当。我们通过给两只雪貂给予浓度分别为0.0%、0.5%和1.0%的异氟烷（isoflurane）后，记录其局部场电位（Local Field Potentials），对该预测进行了验证。实验结果显示，V1脑区与前额叶皮层（PFC）内的源熵在异氟烷作用下显著降低，这与我们的替代性假说预测相符。其中，前额叶皮层的源熵降幅较V1脑区更为显著。V1脑区与前额叶皮层间的信息传递呈双向降低，但从前额叶皮层到V1脑区的降幅更为明显。该结果将信息传递的更强降幅与源熵的更强降幅联系起来，表明源熵降低会减少信息传递。该结论与异氟烷的突触靶点位于局部皮层环路而非脑区间轴突投射所形成突触的观测结果一致。因此，异氟烷作用下的信息传递变化，似乎更源于局部处理过程的改变，而非脑区间的解耦现象。我们提出，在将信息传递变化解读为脑区解耦现象时，必须将源熵的变化纳入考量。