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首页> 外文期刊>The European Journal of Neuroscience >Dendritic calcium mechanisms and long-term potentiation in cortical inhibitory interneurons.
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Dendritic calcium mechanisms and long-term potentiation in cortical inhibitory interneurons.

机译：树突状钙机制和皮质抑制interneurons的长期增强。

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摘要

Calcium (Ca(2+) ) is a major second messenger in the regulation of different forms of synaptic and intrinsic plasticity. Tightly organized in space and time, postsynaptic Ca(2+) transients trigger the activation of many distinct Ca(2+) signaling cascades, providing a means for a highly specific signal transduction and plasticity induction. High-resolution two-photon microscopy combined with highly sensitive synthetic Ca(2+) indicators in brain slices allowed for the quantification and analysis of postsynaptic Ca(2+) dynamics in great detail. Much of our current knowledge about postsynaptic Ca(2+) mechanisms is derived from studying Ca(2+) transients in the dendrites and spines of pyramidal neurons. However, postsynaptic Ca(2+) dynamics differ considerably among different cell types. In particular, distinct rules of postsynaptic Ca(2+) signaling and, accordingly, of Ca(2+) -dependent plasticity operate in GABAergic interneurons. Here, I review recent progress in understanding the complex organization of postsynaptic Ca(2+) signaling and its relevance to several forms of long-term potentiation at excitatory synapses in cortical GABAergic interneurons.
机译：钙（Ca（2+））是调节不同形式的突触和固有可塑性的主要第二信使。在空间和时间上紧密组织，突触后Ca（2+）瞬变触发许多不同的Ca（2+）信号级联的激活，为高度特定的信号转导和可塑性诱导提供了一种手段。高分辨率两光子显微镜与脑片中的高灵敏度合成Ca（2+）指示剂相结合，可以对突触后Ca（2+）动力学进行详细的量化和分析。我们目前有关突触后Ca（2+）机制的许多知识是源于研究锥体神经元的树突和棘中的Ca（2+）瞬变。但是，突触后Ca（2+）动态在不同的细胞类型之间有很大的不同。特别是突触后Ca（2+）信号和相应的Ca（2+）依赖性可塑性的不同规则在GABA能性神经元中起作用。在这里，我回顾了了解突触后Ca（2+）信号的复杂组织及其与皮质GABA能性中间神经元的兴奋性突触的几种形式的长期增强的相关性的最新进展。

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