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The present study was conducted to characterize possible rapid effects of 17-β-estradiol on voltage-gated K +  channels in preoptic neurons and, in particular, to identify the mechanisms by which 17-β-estradiol affects the K +  channels. Whole-cell currents from dissociated rat preoptic neurons were studied by perforated-patch recording. 17-β-estradiol rapidly (within seconds) and reversibly reduced the K +  currents, showing an EC 50  value of 9.7 µM. The effect was slightly voltage dependent, but independent of external Ca 2+ , and not sensitive to an estrogen-receptor blocker. Although 17-α-estradiol also significantly reduced the K +  currents, membrane-impermeant forms of estradiol did not reduce the K +  currents and other estrogens, testosterone and cholesterol were considerably less effective. The reduction induced by estradiol was overlapping with that of the K V -2-channel blocker r-stromatoxin-1. The time course of K +  current in 17-β-estradiol, with a time-dependent inhibition and a slight dependence on external K + , suggested an open-channel block mechanism. The properties of block were predicted from a computational model where 17-β-estradiol binds to open K +  channels. It was concluded that 17-β-estradiol rapidly reduces voltage-gated K +  currents in a way consistent with an open-channel block mechanism. This suggests a new mechanism for steroid action on ion channels.

Mechanism of Estradiol-Induced Block of Voltage-Gated K+ Currents in Rat Medial Preoptic Neurons