Open AccessAstrocytes in Atp1a2 ‐deficient heterozygous mice exhibit hyperactivity after induction of cortical spreading depression
Author(s) -
Sugimoto Hiroki,
Sato Masaaki,
Nakai Junichi,
Kawakami Kiyoshi
Publication year - 2020
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12848
Subject(s) - cortical spreading depression , familial hemiplegic migraine , astrocyte , chemistry , neuroscience , migraine with aura , psychology , aura , medicine , migraine , central nervous system
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.