Cambridge Centre for Frontotemporal Dementia and Related Disorders, Department of Clinical Neurosciences, University of Cambridge, UK; The Wellcome Centre for Human Neuroimaging, UCL Queen Square Institute of Neurology, UK.
The Wellcome Centre for Human Neuroimaging, UCL Queen Square Institute of Neurology, UK.
Neuroimage. 2021 Sep;238:118243. doi: 10.1016/j.neuroimage.2021.118243. Epub 2021 Jun 8.
This technical note introduces adiabatic dynamic causal modelling, a method for inferring slow changes in biophysical parameters that control fluctuations of fast neuronal states. The application domain we have in mind is inferring slow changes in variables (e.g., extracellular ion concentrations or synaptic efficacy) that underlie phase transitions in brain activity (e.g., paroxysmal seizure activity). The scheme is efficient and yet retains a biophysical interpretation, in virtue of being based on established neural mass models that are equipped with a slow dynamic on the parameters (such as synaptic rate constants or effective connectivity). In brief, we use an adiabatic approximation to summarise fast fluctuations in hidden neuronal states (and their expression in sensors) in terms of their second order statistics; namely, their complex cross spectra. This allows one to specify and compare models of slowly changing parameters (using Bayesian model reduction) that generate a sequence of empirical cross spectra of electrophysiological recordings. Crucially, we use the slow fluctuations in the spectral power of neuronal activity as empirical priors on changes in synaptic parameters. This introduces a circular causality, in which synaptic parameters underwrite fast neuronal activity that, in turn, induces activity-dependent plasticity in synaptic parameters. In this foundational paper, we describe the underlying model, establish its face validity using simulations and provide an illustrative application to a chemoconvulsant animal model of seizure activity.
本技术说明介绍了绝热动态因果建模,这是一种推断控制快速神经元状态波动的生物物理参数缓慢变化的方法。我们想到的应用领域是推断脑活动相变(例如阵发性癫痫活动)背后的变量(例如细胞外离子浓度或突触效能)的缓慢变化。该方案效率高,而且由于基于配备参数慢动态(例如突触率常数或有效连通性)的既定神经质量模型,因此保留了生物物理解释。简而言之,我们使用绝热近似来根据隐藏神经元状态(及其在传感器中的表达)的二阶统计量(即它们的复交叉谱)来总结快速波动;即,他们的经验交叉谱。这允许指定和比较生成一系列电生理记录经验交叉谱的慢变参数模型(使用贝叶斯模型简化)。至关重要的是,我们将神经元活动的频谱功率中的缓慢波动用作突触参数变化的经验先验。这引入了循环因果关系,其中突触参数构成了快速神经元活动的基础,而反过来,快速神经元活动又导致突触参数的活性依赖性可塑性。在这篇基础论文中,我们描述了基础模型,使用模拟验证了其表面有效性,并提供了对癫痫活动的化学诱导动物模型的说明性应用。