Impaired electrical signaling disrupts gamma frequency oscillations in connexin 36-deficient mice
Impaired electrical signaling disrupts gamma frequency oscillations in connexin 36-deficient mice
复制标题
DOI：
10.1016/s0896-6273(01)00387-7
复制
发表时间：
2001-08-16
期刊：
影响因子：
16.2
通讯作者：
Monyer, H
中科院分区：
文献类型：
--
作者：
Hormuzdi, SG;Pais, I;Monyer, H
即使是简单的感知任务，神经处理也会在相距较远的皮质区域并行发生。相关的认知结合被认为是通过伽马（30 - 80赫兹）频段节律性活动的区域间同步来实现的。这种振荡是神经网络的一种涌现特性，并且需要常规的化学神经传递。为了测试缝隙连接介导的电信号在这种网络特性中的潜在作用，我们培育出了缺乏连接蛋白36（主要的神经元连接蛋白）的小鼠。在此我们表明，这种蛋白质的缺失会在体外破坏伽马频率的网络振荡，但不影响高频（150赫兹）节律，高频节律可能涉及主细胞之间的缝隙连接（施密茨等人，2001年）。因此，在整个皮质网络中差异分布的特定连接蛋白可能会调节成熟大脑中神经元信息处理的不同功能方面。
Neural processing occurs in parallel in distant cortical areas even for simple perceptual tasks. Associated cognitive binding is believed to occur through the interareal synchronization of rhythmic activity in the gamma (30-80 Hz) range. Such oscillations arise as an emergent property of the neuronal network and require conventional chemical neurotransmission. To test the potential role of gap junction-mediated electrical signaling in this network property, we generated mice lacking connexin 36, the major neuronal connexin. Here we show that the loss of this protein disrupts gamma frequency network oscillations in vitro but leaves high frequency (150 Hz) rhythms, which may involve gap junctions between principal cells (Schmitz et al., 2001), unaffected. Thus, specific connexins differentially deployed throughout cortical networks are likely to regulate different functional aspects of neuronal information processing in the mature brain.