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电信号受损会破坏连接蛋白36缺陷小鼠的γ频率振荡。

Impaired electrical signaling disrupts gamma frequency oscillations in connexin 36-deficient mice.

作者信息

Hormuzdi S G, Pais I, LeBeau F E, Towers S K, Rozov A, Buhl E H, Whittington M A, Monyer H

机构信息

Department of Clinical Neurobiology, University Hospital of Neurology, Im Neuenheimer Feld 364, Heidelberg, Germany.

出版信息

Neuron. 2001 Aug 16;31(3):487-95. doi: 10.1016/s0896-6273(01)00387-7.

DOI:10.1016/s0896-6273(01)00387-7
PMID:11516404
Abstract

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.

摘要

即使是对于简单的感知任务,神经处理也会在远距离的皮质区域并行发生。相关的认知捆绑被认为是通过γ(30 - 80赫兹)范围内节律性活动的区域间同步而发生的。这种振荡作为神经网络的一种涌现特性出现,并且需要传统的化学神经传递。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,我们培育出了缺乏主要神经元连接蛋白36的小鼠。我们在此表明,这种蛋白质的缺失在体外破坏了γ频率的网络振荡,但未影响高频(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。

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