Miller Robert
Otago Centre for Theoretical Studies in Psychiatry and Neuroscience, Department of Anatomy and Structural Biology, School of Medical Science, University of Otago, P.O. Box 913, Dunedin, New Zealand.
Int J Psychophysiol. 2007 Apr;64(1):18-23. doi: 10.1016/j.ijpsycho.2006.07.009. Epub 2006 Sep 25.
The classic alpha rhythm, recorded intracortically, consists of alternating surface-negative troughs and briefer surface-positive peaks. The troughs are associated with neuronal hyperpolarization, the peaks with brief depolarization and burst firing. Each hyperpolarization is mainly a potassium potential, lasting approximately 100 ms. Depolarization and burst firing arise when this inactivates. In the desynchronized state, membrane potential is poised just below threshold. Firing in vivo is somewhat irregular and non-bursting. It is suggested that EEG bistability (classic alpha vs desynchronization) corresponds to bistability of single pyramidal cells. In vitro, paired pulses lead to depression of synaptic transmission in synapses linking two pyramidal cells, but to facilitation in synapses linking pyramidal cells to inhibitory neurones. These effects should be recruited by burst firing in vivo. Thus, enhancement of inhibitory and excitatory transmission occur respectively during the classic alpha rhythm, and the desynchronized state. As a result both states tend to be self-sustaining. In the desynchronized state high frequency (gamma or beta) activity predominates. In simulations, gamma activity has been modeled as the behaviour of cortical networks where populations of excitatory and inhibitory neurones interact. These simulations assume conduction times between neurones to be negligible. However, this is not true for long-distance interactions. Introduction into the models of plausible conduction delays should slow the oscillation frequency. The activated cortex can then produce not only gamma activity but also beta, and sometimes alpha activity. Thus, alpha frequencies can arise both in the "idling" cortex (classic alpha), and in the activated cortex, although the respective mechanisms are quite different.
皮层内记录到的经典α节律由交替出现的表面负向波谷和更短暂的表面正向波峰组成。波谷与神经元超极化相关，波峰与短暂去极化和爆发性放电相关。每次超极化主要是一个钾离子电位，持续约100毫秒。当这种情况失活时会出现去极化和爆发性放电。在去同步化状态下，膜电位刚好处于阈值以下。体内放电有点不规则且非爆发性。有人提出脑电图双稳态（经典α波与去同步化）对应于单个锥体细胞的双稳态。在体外，成对脉冲会导致连接两个锥体细胞的突触中突触传递抑制，但在连接锥体细胞与抑制性神经元的突触中会导致促进。这些效应在体内应通过爆发性放电来募集。因此，在经典α节律和去同步化状态下分别会出现抑制性和兴奋性传递的增强。结果，这两种状态往往都是自我维持的。在去同步化状态下，高频（γ或β）活动占主导。在模拟中，γ活动被建模为兴奋性和抑制性神经元群体相互作用的皮层网络行为。这些模拟假设神经元之间的传导时间可以忽略不计。然而，对于长距离相互作用并非如此。在模型中引入合理的传导延迟应该会减慢振荡频率。然后，激活的皮层不仅可以产生γ活动，还可以产生β活动，有时还可以产生α活动。因此，α频率既可以在“闲置”皮层（经典α波）中出现，也可以在激活的皮层中出现，尽管各自的机制有很大不同。
