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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Reactive oxygen species mediate activity-dependent neuron-glia signaling in output fibers of the hippocampus.
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Reactive oxygen species mediate activity-dependent neuron-glia signaling in output fibers of the hippocampus.

机译:活性氧在海马输出纤维中介导活动相关的神经胶质细胞信号传导。

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摘要

Nonsynaptic signaling is becoming increasingly appreciated in studies of activity-dependent changes in the nervous system. We investigated the types of neuronal activity that elicit nonsynaptic communication between neurons and glial cells in hippocampal output fibers. High-frequency, but not low-frequency, action potential firing in myelinated CA1 axons of the hippocampus resulted in increased phosphorylation of the oligodendrocyte-specific protein myelin basic protein (MBP). This change was blocked by tetrodotoxin, indicating that axonally generated action potentials were necessary to regulate the phosphorylation state of MBP. Furthermore, scavengers of the reactive oxygen species superoxide and hydrogen peroxide and nitric oxide synthase inhibitors prevented activation of this neuron-glia signaling pathway. These results indicate that, during periods of increased neuronal activity in area CA1 of the hippocampus, reactive oxygen and nitrogen species are generated, which diffuse to neighboring oligodendrocytes and result in post-translational modifications of MBP, a key structural protein in myelin. Thus, in addition to their well-known capacity for activity-dependent neuron-neuron signaling, hippocampal pyramidal neurons possess a mechanism for activity-dependent neuron-glia signaling.
机译:在神经系统中与活动有关的变化的研究中,非突触信号越来越受到人们的欢迎。我们调查了引起海马输出纤维中神经元和神经胶质细胞之间非突触通讯的神经元活动的类型。在海马有髓鞘的CA1轴突中高频但非低频的动作电位激发导致少突胶质细胞特异性蛋白髓鞘碱性蛋白(MBP)的磷酸化增加。这种变化被河豚毒素所阻断,表明轴突产生的动作电位对于调节MBP的磷酸化状态是必需的。此外,活性氧超氧化物,过氧化氢和一氧化氮合酶抑制剂的清除剂阻止了该神经元神经胶质信号通路的激活。这些结果表明,在海马CA1区神经元活性增加的期间,会产生活性氧和氮,这些氧和氮扩散到邻近的少突胶质细胞,并导致髓磷脂中关键结构蛋白MBP的翻译后修饰。因此,除了众所周知的活动依赖性神经元神经元信号传导能力外,海马锥体神经元还具有活动依赖性神经元神经胶质信号传导机制。

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