Wei J, Dlouhy S R, Bayer S, Piva R, Verina T, Wang Y, Feng Y, Dupree B, Hodes M E, Ghetti B
Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis 46202-5120, USA.
J Neuropathol Exp Neurol. 1997 Jul;56(7):762-71.
A mutation in the gene Girk2 that encodes an inwardly rectifying potassium channel is the genetic defect causing the behavioral and pathologic abnormalities of the weaver mutant mouse. Of the pathologic abnormalities, the best studied is the neuronal degeneration that occurs in the cerebellar cortex and in the midbrain dopaminergic neurons. A detailed characterization of the topographic and temporal expression of Girk2 is fundamental to elucidate the mechanisms underlying neurodegeneration in these mutant mice. In this study we utilized in situ hybridization to determine the expression of Girk2 mRNA during prenatal and postnatal development in the murine central nervous system (CNS). Girk2 expression was seen in multiple regions of embryonic CNS including the cerebellum and midbrain. During postnatal development, the highest expression was seen in the cerebellum, midbrain and hippocampus. However, since the developing cerebellum undergoes significant neuronal loss due to the degeneration of granule cell precursors, Girk2 mRNA expression in this area decreases progressively.
编码内向整流钾通道的基因Girk2发生突变是导致韦弗突变小鼠行为和病理异常的遗传缺陷。在病理异常中，研究得最充分的是小脑皮质和中脑多巴胺能神经元中发生的神经元变性。详细表征Girk2的拓扑和时间表达对于阐明这些突变小鼠神经变性的潜在机制至关重要。在本研究中，我们利用原位杂交来确定Girk2 mRNA在小鼠中枢神经系统（CNS）产前和产后发育过程中的表达。在胚胎中枢神经系统的多个区域，包括小脑和中脑，都观察到了Girk2的表达。在出生后发育过程中，小脑、中脑和海马中的表达最高。然而，由于发育中的小脑因颗粒细胞前体的变性而经历显著的神经元损失，该区域的Girk2 mRNA表达逐渐降低。
