In:
REPRODUCTION, Bioscientifica, Vol. 143, No. 5 ( 2012-05), p. 625-636
Abstract:
Numerous studies have suggested that K + channels regulate a wide range of physiological processes in mammalian cells. However, little is known about the specific function of K + channels in germ cells. In this study, mouse zygotes were cultured in a medium containing K + channel blockers to identify the functional role of K + channels in mouse embryonic development. Voltage-dependent K + channel blockers, such as tetraethylammonium and BaCl 2 , had no effect on embryonic development to the blastocyst stage, whereas K 2P channel blockers, such as quinine, selective serotonin reuptake inhibitors (fluoxetine, paroxetine, and citalopram), gadolinium trichloride, anandamide, ruthenium red, and zinc chloride, significantly decreased blastocyst formation ( P 〈 0.05). RT-PCR data showed that members of the K 2P channel family, specifically KCNK2, KCNK10, KCNK4, KCNK3, and KCNK9, were expressed in mouse oocytes and embryos. In addition, their mRNA expression levels, except Kcnk3 , were up-regulated by above ninefold in morula-stage embryos compared with 2-cell stage embryos (2-cells). Immunocytochemical data showed that KCNK2, KCNK10, KCNK4, KCNK3, and KCNK9 channel proteins were expressed in the membrane of oocytes, 2-cells, and blastocysts. Each siRNA injection targeted at Kcnk2, Kcnk10, Kcnk4, Kcnk3, and Kcnk9 significantly decreased blastocyst formation by ∼38% compared with scrambled siRNA injection ( P 〈 0.05). The blockade of K 2P channels acidified the intracellular pH and depolarized the membrane potential. These results suggest that K 2P channels could improve mouse embryonic development through the modulation of gating by activators.
Type of Medium:
Online Resource
ISSN:
1470-1626
,
1741-7899
Language:
Unknown
Publisher:
Bioscientifica
Publication Date:
2012
detail.hit.zdb_id:
2037813-0
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