Role of Tau Protein on Neocortical and Hippocampal Oscillatory Patterns
Role of Tau Protein on Neocortical and Hippocampal Oscillatory Patterns
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DOI：
10.1002/hipo.20798
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发表时间：
2011-08-01
期刊：
影响因子：
3.5
通讯作者：
Avila, Jesus
中科院分区：
文献类型：
--
作者：
Cantero, Jose L.;Moreno-Lopez, Bernardo;Avila, Jesus
Tau是一种神经元微管相关蛋白，参与神经元形态发生过程中微管的稳定、轴突的建立和伸长。由于其在新皮层区域和海马中的表达升高，tau可能在塑造集体神经反应中发挥作用，这些反应是海马和新皮层之间的慢和快脑振荡和/或长距离同步模式的基础。为了验证这一假设，在自发运动探索行为期间，在tau缺陷（tau（-/-））和野生型小鼠中记录来自不同新皮质区域和来自海马的局部场电位。我们发现，tau蛋白（-/-）小鼠表现出海马theta减慢和涉及额叶皮层的伽马长程同步水平降低。我们假设，在发展的早期阶段缺乏正常的磷酸化tau蛋白可能会影响小白蛋白中间神经元的成熟，影响远程伽马同步的时空结构。此外，间隙连接通道的正常功能可能会受到海马网络中tau蛋白缺失的影响。总之，这些结果提供了新的见解tau蛋白的功能作用，在形成集体神经反应和出现的哺乳动物大脑中的新皮质-海马相互作用。(C)2010 Wiley-Liss，Inc.
Tau is a neuronal microtubule-associated protein implicated in microtubules stabilization, axonal establishment and elongation during neuronal morphogenesis. Because of its elevated expression in neocortical regions and hippocampus, tau might play a role in sculpting collective neural responses underlying slow and fast brain oscillations and/or long-range synchronization patterns between hippocampus and neocortex. To test this hypothesis, local field potentials were recorded in tau-deficient (tau(-/-)) and wild-type mice from different neocortical regions and from the hippocampus during spontaneous motor exploratory behavior. We found that tau(-/-) mice showed hippocampal theta slowing and reduced levels of gamma long-range synchronization involving the frontal cortex. We hypothesize that the lack of normal phosphorylated tau during early stages of development might influence the maturation of parvalbumin interneurons affecting the spatiotemporal structure of long-range gamma synchronization. Also, the proper functioning of gap-junction channels might be compromised by the absence of tau in hippocampal networks. Altogether, these results provide novel insights into the functional role of tau protein in the formation of collective neural responses and emergence of neocortical-hippocampal interactions in the mammalian brain. (C) 2010 Wiley-Liss, Inc.