Astrocytes in Atp1a2‐deficient heterozygous mice exhibit hyperactivity after induction of cortical spreading depression
Astrocytes in Atp1a2‐deficient heterozygous mice exhibit hyperactivity after induction of cortical spreading depression
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Atp1a2 缺陷杂合小鼠的星形胶质细胞在诱导皮质扩散抑制后表现出过度活跃
DOI：
10.1002/2211-5463.12848
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发表时间：
2020
期刊：
影响因子：
2.6
通讯作者：
Junichi Nakai and Kiyoshi Kawakami
中科院分区：
文献类型：
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作者：
Hiroki Sugimoto;Masaaki Sato;Junichi Nakai and Kiyoshi Kawakami
ATP 1A 2编码Na，K-ATP酶α2亚基，主要定位于星形胶质细胞，是家族性偏瘫型偏头痛2型（FHM 2）的致病基因。FHM 2模型小鼠（Atp 1a 2 tmCKwk/+）易患皮质扩散性抑制（CSD），其与偏头痛先兆和头痛深刻相关。然而，CSD期间的星形胶质细胞特性尚未在FHM 2模型小鼠中进行检查。使用Atp 1a 2 tmCKwk/+与在皮层神经元和星形胶质细胞中表达G-CaMP 7的转基因小鼠（Atp 1a 2 +/−）杂交，我们分析了CSD期间Ca 2+浓度的变化。在Atp 1a 2 +/−中，Ca 2+波的传播速度和具有升高的Ca 2+浓度的星形胶质细胞的百分比高于野生型小鼠。在Atp 1a 2 +/−条件下，随着钙离子浓度升高，星形胶质细胞的百分比增加，这可能与FHM 2的病理生理学有关。
TheATP1A2coding α2 subunit of Na,K‐ATPase, which is predominantly located in astrocytes, is a causative gene of familial hemiplegic migraine type 2 (FHM2). FHM2 model mice (Atp1a2tmCKwk/+) are susceptible to cortical spreading depression (CSD), which is profoundly related to migraine aura and headache. However, astrocytic properties during CSD have not been examined in FHM2 model mice. UsingAtp1a2tmCKwk/+crossed with transgenic mice expressing G‐CaMP7 in cortical neurons and astrocytes (Atp1a2+/−), we analyzed the changes in Ca2+concentrations during CSD. The propagation speed of Ca2+waves and the percentages of astrocytes with elevated Ca2+concentrations inAtp1a2+/−were higher than those in wild‐type mice. Increased percentages of astrocytes with elevated Ca2+concentrations inAtp1a2+/−may contribute to FHM2 pathophysiology.