Astrocytes in Atp1a2-deficient heterozygous mice exhibit hyperactivity after induction of cortical spreading depression

在Atp1a2缺陷型杂合子小鼠中,皮层扩散性抑制诱导后,星形胶质细胞表现出过度活跃。

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Abstract

The ATP1A2 coding 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 (Atp1a2(tmCKwk/+) ) 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. Using Atp1a2(tmCKwk/+) crossed with transgenic mice expressing G-CaMP7 in cortical neurons and astrocytes (Atp1a2(+/-) ), we analyzed the changes in Ca(2+) concentrations during CSD. The propagation speed of Ca(2+) waves and the percentages of astrocytes with elevated Ca(2+) concentrations in Atp1a2(+/-) were higher than those in wild-type mice. Increased percentages of astrocytes with elevated Ca(2+) concentrations in Atp1a2(+/-) may contribute to FHM2 pathophysiology.

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