文章基本信息

标题：Intracerebroventricular antisense knockdown of Gα i2 results in ciliary stasis and ventricular dilatation in the rat
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作者：Kati S Mönkkönen ; Juhana M Hakumäki ; Robert A Hirst 等
期刊名称：BMC Neuroscience
印刷版ISSN：1471-2202
电子版ISSN：1471-2202
出版年度：2007
卷号：8
期号：1
页码：1
DOI：10.1186/1471-2202-8-26
语种：English
出版社：BioMed Central
摘要：Background In the CNS, the heterotrimeric G protein Gα_i2 is a minor Gα subunit with restricted localization in the ventricular regions including the ependymal cilia. The localization of Gα_i2 is conserved in cilia of different tissues, suggesting a particular role in ciliary function. Although studies with Gα_i2-knockout mice have provided information on the role of this Gα subunit in peripheral tissues, its role in the CNS is largely unknown. We used intracerebroventricular (icv) antisense administration to clarify the physiological role of Gα_i2 in the ventricular system. Results High resolution MRI studies revealed that continuous icv-infusion of Gα_i2-specific antisense oligonucleotide caused unilateral ventricular dilatation that was restricted to the antisense-receiving ventricle. Microscopic analysis demonstrated ependymal cell damage and loss of ependymal cilia. Attenuation of Gα_i2 in ependymal cells was confirmed by immunohistochemistry. Ciliary beat frequency measurements on cultured ependymal cells indicated that antisense administration resulted in ciliary stasis. Conclusion Our results establish that Gα_i2 has an essential regulatory role in ciliary function and CSF homeostasis.