High Performance Computing Centre, University of Canterbury, New Zealand.
High Performance Computing Centre, University of Canterbury, New Zealand.
Neuroimage. 2018 Jul 1;174:69-86. doi: 10.1016/j.neuroimage.2018.03.010. Epub 2018 Mar 8.
A state-of-the-art integrated model of neurovascular coupling (NVC) (Dormanns et al., 2015b; Dormanns et al., 2016; Kenny et al., 2018) and the BOLD response (Mathias et al., 2017a; Mathias et al., 2017b) is presented with the ability to simulate the fMRI BOLD responses due to continuous neuronal spiking, bursting and cortical spreading depression (CSD) along with the underlying complex vascular coupling. Simulated BOLD responses are compared to experimental BOLD signals observed in the rat barrel cortex and in the hippocampus under seizure conditions showing good agreement. Bursting phenomena provides relatively clear BOLD signals as long as the time between bursts is not too short. For short burst periods the BOLD signal remains constant even though the neuron is in a predominantly bursting mode. Simulation of CSD exhibits large negative BOLD signals. Visco-elastic effects of the capillary bed do not seem to have a large effect on the BOLD signal even for relatively high values of oxygen consumption. While the results of the model suggests that potassium ions released during neural activity could act as the main mediator in NVC, it suggests the possibility of other mechanisms that can coexist and increase blood flow such as the arachidonic acid to epoxyeicosatrienoic acid (EET) pathway. The comparison with experimental cerebral blood flow (CBF) data indicates the possible existence of multiple neural pathways influencing the vascular response. Initial negative BOLD signals occur for all simulations due to the rate at which the metabolic oxygen consumption occurs relative to the dilation of the perfusing cerebro-vasculature. However it is unclear as to whether these are normally seen clinically due to the size of the magnetic field. Experimental comparisons for different animal experiments may very well require variation in the model parameters. The complex integrated model is believed to be the first of its kind to simulate both NVC and the resulting BOLD signal.
提出了一种神经血管耦合（NVC）的最先进的综合模型（Dormanns 等人，2015b；Dormanns 等人，2016；Kenny 等人，2018）和 BOLD 响应（Mathias 等人，2017a；Mathias 等人，2017b），能够模拟由于连续神经元放电、爆发和皮质扩散性抑制（CSD）以及潜在的复杂血管耦合引起的 fMRI BOLD 响应。模拟的 BOLD 响应与在癫痫发作条件下在大鼠皮层桶状结构和海马中观察到的实验 BOLD 信号进行了比较，显示出良好的一致性。只要爆发之间的时间间隔不是太短，爆发现象就会提供相对清晰的 BOLD 信号。对于短暂的爆发周期，即使神经元处于主要爆发模式，BOLD 信号仍保持不变。CSD 的模拟表现出较大的负 BOLD 信号。毛细血管床的粘弹性效应似乎对 BOLD 信号没有太大影响，即使耗氧量相对较高。虽然模型的结果表明，在神经活动过程中释放的钾离子可能是 NVC 的主要介导物，但它表明可能存在其他机制可以共存并增加血流量，例如花生四烯酸至环氧二十碳三烯酸（EET）途径。与实验脑血流（CBF）数据的比较表明，可能存在多种影响血管反应的神经通路。由于代谢耗氧量与灌注脑血管扩张的相对速率，所有模拟都会产生初始的负 BOLD 信号。然而，由于磁场的大小，尚不清楚这些信号在临床上是否正常出现。对于不同的动物实验，实验比较可能非常需要改变模型参数。该综合模型被认为是第一个能够模拟 NVC 和由此产生的 BOLD 信号的模型。
