Data from: 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.

大脑区域间耦合的中断被认为是麻醉状态下意识丧失的潜在机制。此前已有研究通过测量大脑区域间的信息传递，并将信息传递减弱作为脑区间解耦的替代指标，对该假说展开验证。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，即使耦合未发生改变，信息传递也会随之下降。因此，我们重新审视了此前将信息传递减弱解读为解耦信号的结论，并探讨受损的局部信息处理是否会导致信息传递丧失。这一替代假说的一项重要预测是，局部可用信息量（信号熵，signal entropy）的变化至少应与信息传递的变化同样显著。我们通过向两只雪貂给予0.0%、0.5%和1.0%浓度的异氟烷（isoflurane），随后记录其局部场电位（local field potentials），对这一预测进行了验证。我们发现，在V1区与前额叶皮层（prefrontal cortex, PFC）中，异氟烷作用下的源熵（source entropy）显著下降——这与我们的替代假说预测一致。前额叶皮层的源熵下降幅度较V1区更为显著。V1区与前额叶皮层间的信息传递呈双向减弱，但从前额叶皮层到V1区的下降幅度更大。这一结果将信息传递的更强减弱与源熵的更强下降联系起来，表明源熵的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的突触这一观测结果相符。因此，异氟烷作用下的信息传递变化，似乎更像是局部处理过程改变的结果，而非大脑区域间解耦的表现。我们建议，在将信息传递变化解读为解耦信号时，必须考虑源熵的变化。