Novel plasma membrane action of estrogen and antiestrogens revealed by their regulation of a large conductance chloride channel

FASEB J. 1994 Jul;8(10):760-5. doi: 10.1096/fasebj.8.10.8050676.


Antiestrogens antagonize many genomic effects of estrogen through binding to the nuclear estrogen receptor. We report here that NIH3T3 fibroblasts grown in the presence of colchicine acquire the activation of a large conductance chloride channel upon exposure to extracellular but not intracellular antiestrogens. This effect can be prevented by extracellular 17 beta-estradiol, but not intracellular 17 beta-estradiol or extracellular 17 alpha-estradiol. This is the first demonstration of a regulatory role for antiestrogens and estrogens in the regulation of ionic channels occurring through an interaction of these compounds with a plasma membrane binding site distinct from the classical estrogen receptor and subsequent activation of intracellular second messenger pathway (or pathways).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Membrane / drug effects
  • Cell Membrane / physiology
  • Chloride Channels / drug effects*
  • Chloride Channels / physiology
  • Colchicine
  • Estradiol / pharmacology*
  • Humans
  • Membrane Potentials
  • Mice
  • Toremifene / pharmacology*


  • Chloride Channels
  • Estradiol
  • Toremifene
  • Colchicine