A nonsynaptic mechanism underlying interictal discharges in human epileptic neocortex
A nonsynaptic mechanism underlying interictal discharges in human epileptic neocortex
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DOI：
10.1073/pnas.0912652107
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发表时间：
2010-01-05
影响因子：
11.1
通讯作者：
Cunningham, Mark O.
中科院分区：
文献类型：
--
作者：
Roopun, Anita K.;Simonotto, Jennifer D.;Cunningham, Mark O.
非常快的振荡（VFO，>80 Hz）对于大脑的生理过程非常重要，过度的振荡对于某些癫痫症也很重要。 VFO 的假定机制包括中间神经元尖峰和耦合锥体细胞轴突中的网络活动。目前尚不清楚这些中的任何一个或两者是否适用于病理生理条件。自发发生的发作间期放电发生在体外从新皮质癫痫病灶切除的人体组织中。与这些放电相关的 VFO 在场电位和相位延迟的情况下，在快速尖峰中间神经元的兴奋性突触输入中都很明显。体细胞锥体细胞和中间神经元尖峰的募集较低，VFO 功率和主细胞突触输入之间没有相关性。减少突触抑制并不能影响 VFO 的发生，但它们可以通过减少间隙连接电导而消除。这些数据表明中间神经元缺乏因果作用，并支持癫痫人类新皮质中 VFO 的非突触锥体细胞网络起源。
Very fast oscillations (VFOs, >80 Hz) are important for physiological brain processes and, in excess, with certain epilepsies. Putative mechanisms for VFO include interneuron spiking and network activity in coupled pyramidal cell axons. It is not known whether either, or both, of these apply in pathophysiological conditions. Spontaneously occurring interictal discharges occur in human tissue in vitro, resected from neocortical epileptic foci. VFO associated with these discharges was manifest in both field potential and, with phase delay, in excitatory synaptic inputs to fast spiking interneurons. Recruitment of somatic pyramidal cell and interneuron spiking was low, with no correlation between VFO power and synaptic inputs to principal cells. Reducing synaptic inhibition failed to affect VFO occurrence, but they were abolished by reduced gap junction conductance. These data suggest a lack of a causal role for interneurons, and favor a nonsynaptic pyramidal cell network origin for VFO in epileptic human neocortex.