Experimental Neurology Group, Nuffield Department of Clinical Neuroscience, University of Oxford, Oxford, OX3 9DU, UK.
Eur J Neurosci. 2014 Jun;39(11):1951-9. doi: 10.1111/ejn.12574. Epub 2014 Apr 3.
Oscillatory activity in the beta (13-30 Hz) frequency band is widespread in cortico-basal ganglia circuits, and becomes prominent in Parkinson's disease (PD). Here we develop the hypothesis that the degree of synchronization in this frequency band is a critical factor in gating computation across a population of neurons, with increases in beta band synchrony entailing a loss of information-coding space and hence computational capacity. Task and context drive this dynamic gating, so that for each state there will be an optimal level of network synchrony, and levels lower or higher than this will impair behavioural performance. Thus, both the pathological exaggeration of synchrony, as observed in PD, and the ability of interventions like deep brain stimulation (DBS) to excessively suppress synchrony can potentially lead to impairments in behavioural performance. Indeed, under physiological conditions, the manipulation of computational capacity by beta activity may itself present a mechanism of action selection and maintenance.
在皮质-基底神经节回路中，β（13-30 Hz）频段的振荡活动广泛存在，并在帕金森病（PD）中变得突出。在这里，我们提出了一个假设，即该频段的同步程度是在神经元群体中进行门控计算的关键因素，β 频段同步的增加意味着信息编码空间的丧失，因此计算能力降低。任务和上下文驱动这种动态门控，因此对于每种状态，都会有一个最佳的网络同步水平，低于或高于该水平将损害行为表现。因此，PD 中观察到的同步过度放大以及深部脑刺激（DBS）等干预措施过度抑制同步的能力都可能导致行为表现受损。事实上，在生理条件下，β 活动对计算能力的操纵本身可能是一种作用选择和维持的机制。
