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首页> 外文期刊>The European Journal of Neuroscience >Q/R editing of the rat GluR5 and GluR6 kainate receptors in vivo and in vitro: evidence for independent developmental, pathological and cellular regulation.
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Q/R editing of the rat GluR5 and GluR6 kainate receptors in vivo and in vitro: evidence for independent developmental, pathological and cellular regulation.

机译：体内和体外对大鼠GluR5和GluR6海藻酸酯受体的Q / R编辑：独立发育，病理学和细胞调节的证据。

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Kainate (KA) is a potent neuroexcitatory agent in several areas of the adult brain, with convulsant and excitotoxic properties that increase as ontogeny proceeds. Besides its depolarizing actions, KA may enhance intracellular accumulation of Ca2+ to promote selective neuronal damage. The effects of KA are mediated by specific receptors recently considered to be involved in fast neurotransmission and that can be activated synaptically. KA receptors, e.g. GluR5 and GluR6 have been characterized by molecular cloning. Structure-function relationships indicate that in the MII domain of these KA receptors, a glutamine (Q) or arginine (R) residue determines ion selectivity. The arginine stems from post-transcriptional editing of the GluR5 and GluR6 pre-RNAs, and the unedited and edited versions of GluR6 elicit distinct Ca2+ permeability. Using a PCR-based approach, we show that in vivo, Q/R editing in the GluR5 and GluR6 mRNAs is modulated during ontogeny and differs substantially in a variety of nervous tissues. GluR5 editing is highest in peripheral nervous tissue, e.g. the dorsal root ganglia, where GluR6 expression is barely detectable. In contrast, GluR6 editing is maximal in forebrain and cerebellar structures where GluR5 editing is lower. Intra-amygdaloid injections of KA provide a model of temporal lobe epilepsy, and we show that following seizures, the extent of GluR5 and GluR6 editing is altered in the hippocampus. However, in vitro, high levels of glutamate and potassium-induced depolarizations have no effect on GluR5 and GluR6 Q/R editing. GluR6 editing is rapidly enhanced to maximal levels in primary cultures of cerebellar granule neurons but not in cultured hippocampal pyramidal neurons. Finally, we show that cultured glial cells express partially edited GluR6 mRNAs. Our results indicate that Q/R editing of GluR5 and GluR6 mRNAs is structure-, cell type- and time-dependent, and suggest that editing of these mRNAs is not co-regulated.
机译：海藻酸盐（KA）在成年大脑的多个区域是一种有效的神经兴奋剂，具有惊厥和兴奋毒性，随着个体发育的进行而增加。除了其去极化作用外，KA还可以增强细胞内Ca2 +的积累，从而促进选择性神经元损伤。 KA的作用由最近被认为参与快速神经传递并且可以被突触激活的特定受体介导。 KA受体，例如GluR5和GluR6已通过分子克隆进行了表征。结构-功能关系表明，在这些KA受体的MII域中，谷氨酰胺（Q）或精氨酸（R）残基决定了离子选择性。精氨酸源于GluR5和GluR6前RNA的转录后编辑，而GluR6的未经编辑和编辑的版本则引起不同的Ca2 +渗透性。使用基于PCR的方法，我们表明在体内，在个体发育过程中，GluR5和GluR6 mRNA中的Q / R编辑受到调节，并且在多种神经组织中存在显着差异。 GluR5编辑在周围神经组织中最高，例如背根神经节，几乎检测不到GluR6表达。相反，在GluR5编辑度较低的前脑和小脑结构中，GluR6编辑度最大。杏仁内注射KA提供了颞叶癫痫的模型，我们显示癫痫发作后，海马中GluR5和GluR6编辑的程度发生了改变。但是，在体外，高水平的谷氨酸和钾诱导的去极化对GluR5和GluR6 Q / R编辑没有影响。在小脑颗粒神经元的原代培养中，GluR6编辑迅速增强到最大水平，而在培养的海马锥体神经元中则没有。最后，我们显示培养的神经胶质细胞表达部分编辑的GluR6 mRNA。我们的结果表明，GluR5和GluR6 mRNA的Q / R编辑是结构，细胞类型和时间依赖性的，并且表明这些mRNA的编辑不受共同调节。

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