Epileptiform spikes desynchronize and diminish fast (gamma) activity of the brain - An "anti-binding" mechanism?
Epileptiform spikes desynchronize and diminish fast (gamma) activity of the brain - An "anti-binding" mechanism?
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DOI：
10.1016/s0361-9230(02)00768-2
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发表时间：
2002-05-01
影响因子：
3.8
通讯作者：
Medvedev, AV
中科院分区：
文献类型：
--
作者：
Medvedev, AV
大脑电活动的快速（20- 100 Hz）节律已经被认为对感知和认知很重要，为心理表征下的神经活动的时间绑定提供了机制。此外，在患者和一些实验模型中，快节律通常先于癫痫样放电。在大鼠中，全身性红藻氨酸（KA）后的普遍缓慢（2- 3 Hz）峰电位活动已被证明是由强烈的γ活动引起的。在红藻氨酸诱导的急性癫痫发生过程中，研究了增强的γ节律和随后的棘波活动之间的关系。在1- 100 Hz频率范围内，分析了从大鼠大脑皮层-新皮层结构记录的EEG的功率、多重相干性和相位。伽马节律，放电开始时非常强烈和高度一致！随后出现癫痫样棘波/尖波的缓慢节律。在此尖峰活动期间和之后立即，伽马功率和相干性显着降低。这些数据表明，γ节律和尖峰活动之间的拮抗作用，后者的能力，deserminize和抑制前者。他们是支持的假设，癫痫样穗活动可能导致极端激活的“反结合”机制控制时间结合在高频率。这表明，当快速活动异常增强，“过度绑定”与全球同步的伽马节律可以发生在神经网络。它可能导致突触修饰不足。为了防止这一过程，癫痫样放电发展为抑制快速活动的保护机制。这一提议对我们理解大脑中的时间绑定以及其过度激活如何加速病理状态的发展具有影响。(C)2002年爱思唯尔科学公司All rights reserved.
Fast (20-100Hz) rhythms of electrical activity of the brain have been suggested to be important for perception and cognition providing a mechanism for temporal binding of neural activities underlying mental representations. Also, fast rhythms often precede epileptiform discharges in patients and some experimental models. Generalized slow (2-3Hz) spike activity after systemic kainic acid (KA) in the rat has been shown to be preceded by intense gamma activity. A relationship between the intensified gamma rhythms and the subsequent spike activity was studied during kainate-induced acute epileptogenesis. Power, multiple coherence and phase were analyzed at frequencies 1-100Hz in the EEG recorded from the hippocampal-neocortical structures of the rat. Gamma rhythms, extremely intense and highly coherent at the onset of discharges! were followed by a slow rhythm of epileptiform spikes/sharp waves. During this spike activity and immediately afterwards, the gamma power and coherence were significantly decreased. These data show an antagonism between gamma rhythms and spike activity and ability of the latter to desynchronize and suppress the former. They are supportive to the hypothesis that epileptiform spike activity may result from the extreme activation of the "anti-binding" mechanism controlling temporal binding at high frequencies. It is suggested that when fast activity is abnormally intensified, "over-binding" with global synchrony of gamma rhythms can occur in the neural networks. It may lead to inadequate synaptic modifications. To prevent this process, epileptiform discharge develops as a protective mechanism suppressing fast activity. This proposal has implications for our understanding of temporal binding in the brain and how its excessive activation may precipitate the development of pathological states. (C) 2002 Elsevier Science Inc. All rights reserved.