NDLI: Okadaic acid-sensitive activation of Maxi Cl− channels by triphenylethylene antioestrogens in C1300 mouse neuroblastoma cells

Content Provider	PubMed Central
Author	Diaz, Mario Lock, Hagar Muñoz, Francisco J. Hardy, Simon P. Posas, Francesc Valverde, Miguel A. Bahamonde, Maria I.
Copyright Year	2001
Abstract	The regulation of Maxi Cl− channels by 17β-oestradiol and non-steroidal triphenylethylene antioestrogens represents a rapid, non-classical effect of these compounds. In the present study we have investigated the signalling pathways used for the regulation of Maxi Cl− channel activity by oestrogens and antioestrogens in C1300 neuroblastoma cells. Whole-cell Maxi Cl− currents were readily and reversibly activated by tamoxifen, toremifene and the membrane-impermeant ethyl-bromide tamoxifen, only when applied to the extracellular medium. Pre-treatment of C1300 cells with oestrogen or cAMP prevented the antioestrogen-induced activation of Maxi Cl− channels. The inhibitory effect of 17β-oestradiol and cAMP was abolished by the kinase inhibitor staurosporine. Current activation was unaffected by the removal of intracellular Ca2+ and Mg2+, but was completely abolished in the presence of okadaic acid. These results are consistent with the participation of an okadaic acid-sensitive serine/threonine protein phosphatase in the activation of Maxi Cl− channels. However, neither oestrogen or antioestrogen treatment modified the total activity of the two major serine/threonine phosphatases, PP1 and PP2A, in C1300 cells. Although the role of these Maxi Cl− channels remains unknown, our findings suggest strongly that their modulation by oestrogens and antioestrogens is linked to intracellular signalling pathways.
Related Links	http://dx.doi.org/10.1111/j.1469-7793.2001.00079.x
Ending Page	88
Page Count	10
Starting Page	79
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 1
Volume Number	536
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2001-10-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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