Womack M, Thompson K, Fanselow E, Augustine G J, Peterson A
Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.
Neuroreport. 1998 Oct 26;9(15):3391-5. doi: 10.1097/00001756-199810260-00011.
Weaver mice carry a mutation in the pore domain of the Girk2 (Kcnj6) gene. The mutation causes GIRK2 containing channels to lose ion selectivity and to become constitutively active. It is not known how this alteration in ion channel activity causes in cerebellar granule cells the defects in neurite extension, cell migration and induction of cell death that are characteristic of weaver mice. One possibility is that the mutation causes an inability to regulate intracellular calcium levels properly. We tested this hypothesis by measuring intracellular calcium levels in granule cells and Purkinje cells in slices from the cerebellum of weaver mice. We report here that weaver mice have increases in resting calcium levels in their granule cells, which may account for the multiple effects of the weaver mutation upon these cells.
韦弗氏小鼠在Girk2（Kcnj6）基因的孔道结构域携带一种突变。该突变导致含有GIRK2的通道丧失离子选择性并持续激活。目前尚不清楚离子通道活性的这种改变如何在小脑颗粒细胞中导致韦弗氏小鼠特有的神经突延伸、细胞迁移和细胞死亡诱导缺陷。一种可能性是该突变导致无法正常调节细胞内钙水平。我们通过测量韦弗氏小鼠小脑切片中颗粒细胞和浦肯野细胞的细胞内钙水平来检验这一假设。我们在此报告，韦弗氏小鼠颗粒细胞的静息钙水平升高，这可能解释了韦弗氏突变对这些细胞的多种影响。
