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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Role of the alpha1G T-type calcium channel in spontaneous absence seizures in mutant mice.
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Role of the alpha1G T-type calcium channel in spontaneous absence seizures in mutant mice.

机译：alpha1G T型钙通道在突变小鼠自发性癫痫发作中的作用。

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摘要

Alterations in thalamic T-type Ca2+ channels are thought to contribute to the pathogenesis of absence seizures. Here, we found that mice with a null mutation for the pore-forming alpha1A subunits of P/Q-type channels (alpha1A-/- mice) were prone to absence seizures characterized by typical spike-and-wave discharges (SWDs) and behavioral arrests. Isolated thalamocortical relay (TC) neurons from these mice showed increased T-type Ca2+ currents in vitro. To examine the role of increased T-currents in alpha1A-/- TC neurons, we cross-bred alpha1A-/- mice with mice harboring a null mutation for the gene encoding alpha1G, a major isotype of T-type Ca2+ channels in TC neurons. alpha1A-/-/alpha1G-/- mice showed a complete loss of T-type Ca2+ currents in TC neurons and displayed no SWDs. Interestingly, alpha1A-/-/alpha1G+/- mice had 75% of the T-type Ca2+ currents in TC neurons observed in alpha1A+/+/alpha1G+/+ mice and showed SWD activity that was quantitatively similar to that in alpha1A-/-/alpha1G+/+ mice. Similar results were obtained using double-mutant mice harboring the alpha1G mutation plus another mutation also used as a model for absence seizures, i.e., lethargic (beta4(lh/lh)), tottering (alpha1A(tg/tg)), or stargazer (gamma2(stg/stg)). The present results reveal that alpha1G T-type Ca2+ channels play a critical role in the genesis of spontaneous absence seizures resulting from hypofunctioning P/Q-type channels, but that the augmentation of thalamic T-type Ca2+ currents is not an essential step in the genesis of absence seizures.
机译：丘脑T型Ca2 +通道的改变被认为与失神发作有关。在这里，我们发现P / Q型通道的成孔alpha1A亚基具有无效突变的小鼠（alpha1A-/-小鼠）容易出现癫痫发作，其特征在于典型的波峰放电（SWD）和行为逮捕。从这些小鼠分离的丘脑皮质中继（TC）神经元在体外显示出增加的T型Ca2 +电流。若要检查增加的T电流在alpha1A-/-TC神经元中的作用，我们将alpha1A-/-小鼠与对编码alpha1G的基因具有无效突变的小鼠进行了杂交，alpha1G是TC神经元中T型Ca2 +通道的主要同种型。 alpha1A-/-// alpha1G-/-小鼠在TC神经元中显示出T型Ca2 +电流的完全丧失，并且没有显示SWD。有趣的是，alpha1A-/-// alpha1G +/-小鼠在alpha1A + / + / alpha1G + / +小鼠中观察到TC神经元中T型Ca2 +电流的75％，并且其SWD活性与alpha1A-/-/的定量相似alpha1G + / +小鼠。使用携带alpha1G突变的双突变小鼠以及另一个也用作失神发作的模型的突变获得了相似的结果，即嗜睡（beta4（lh / lh）），蹒跚（alpha1A（tg / tg））或观星者（ gamma2（stg / stg））。目前的结果表明，α1GT型Ca2 +通道在功能低下的P / Q型通道导致的自发性癫痫发作的发生中起着关键作用，但是丘脑T型Ca2 +电流的增加并不是该过程中的必要步骤。失神发作的起源。

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