Voytek Bradley, Knight Robert T
Department of Cognitive Science, Neurosciences Graduate Program, and the Institute for Neural Computation, University of California, San Diego, La Jolla, California..
Department of Psychology and Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, California.
Biol Psychiatry. 2015 Jun 15;77(12):1089-97. doi: 10.1016/j.biopsych.2015.04.016. Epub 2015 Apr 28.
Perception, cognition, and social interaction depend upon coordinated neural activity. This coordination operates within noisy, overlapping, and distributed neural networks operating at multiple timescales. These networks are built upon a structural scaffolding with intrinsic neuroplasticity that changes with development, aging, disease, and personal experience. In this article, we begin from the perspective that successful interregional communication relies upon the transient synchronization between distinct low-frequency (<80 Hz) oscillations, allowing for brief windows of communication via phase-coordinated local neuronal spiking. From this, we construct a theoretical framework for dynamic network communication, arguing that these networks reflect a balance between oscillatory coupling and local population spiking activity and that these two levels of activity interact. We theorize that when oscillatory coupling is too strong, spike timing within the local neuronal population becomes too synchronous; when oscillatory coupling is too weak, spike timing is too disorganized. Each results in specific disruptions to neural communication. These alterations in communication dynamics may underlie cognitive changes associated with healthy development and aging, in addition to neurological and psychiatric disorders. A number of neurological and psychiatric disorders-including Parkinson's disease, autism, depression, schizophrenia, and anxiety-are associated with abnormalities in oscillatory activity. Although aging, psychiatric and neurological disease, and experience differ in the biological changes to structural gray or white matter, neurotransmission, and gene expression, our framework suggests that any resultant cognitive and behavioral changes in normal or disordered states or their treatment are a product of how these physical processes affect dynamic network communication.
感知、认知和社会互动依赖于协调的神经活动。这种协调在嘈杂、重叠且分布于多个时间尺度上运作的神经网络中进行。这些网络建立在具有内在神经可塑性的结构支架之上，而这种可塑性会随着发育、衰老、疾病和个人经历而改变。在本文中，我们从这样一种观点出发：成功的区域间通信依赖于不同低频（<80Hz）振荡之间的瞬时同步，从而通过相位协调的局部神经元放电实现短暂的通信窗口。据此，我们构建了一个动态网络通信的理论框架，认为这些网络反映了振荡耦合与局部群体放电活动之间的平衡，且这两种活动水平相互作用。我们推测，当振荡耦合过强时，局部神经元群体内的放电时间会变得过于同步；当振荡耦合过弱时，放电时间则过于紊乱。每种情况都会导致神经通信的特定中断。除了神经和精神疾病外，这些通信动态的改变可能是与健康发育和衰老相关的认知变化的基础。许多神经和精神疾病——包括帕金森病、自闭症、抑郁症、精神分裂症和焦虑症——都与振荡活动异常有关。尽管衰老、精神和神经疾病以及经历在结构灰质或白质、神经传递和基因表达的生物学变化方面存在差异，但我们的框架表明，正常或紊乱状态下任何由此产生的认知和行为变化或其治疗都是这些物理过程如何影响动态网络通信的产物。
