17-b-Estradiol Modulation of Area Postrema Potassium Currents

Li, Zhicheng and Meredith Hay. 17-b-Estradiol modulation of area postrema potassium currents. J Neurophysiol 84: 1385–1391, 2000. The purpose of this study was to determine the effects of 17-bestradiol on area postrema neuronal activity in vivo and on area postrema potassium currents (IK) in vitro. In anesthetized rats, intravenous injection of 17-b-estradiol (10 ng/kg bw) -inhibited area postrema neuronal activity in 8/8 neurons tested. The averaged firing rate decreased from 2.9 6 1.1 to 1.1 6 0.3 Hz. The inhibitory effects of 17-b-estradiol on area postrema neuronal activity were rapid in onset (within 1 min) and long-lasting (.8 min). To study the cellular mechanisms involved in this response, the effects of 17-b-estradiol were examined in dissociated area postrema neurons. In these cells, 17-b-estradiol (0.5 nM) increased the averaged peak IK 27 6 8%. The time course for the potentiation was observed within ;0.5–1 min after the application of 17-b-estradiol. Full recovery from the potentiation usually occurred within ;3–4 min after the washout of 17-b-estradiol. The biologically inactive 17-a-estradiol had no effect on area postrema IK and the 17-b-estradiol antagonist, ICI 182,780 blocked the effects of 17-b-estradiol on area postrema IK. Finally, big conductance calcium-activated potassium current (MaxiK) was identified in area postrema neurons (n 5 12/12). Blockade of MaxiK with 100 nM iberiotoxin blocked the effects of 17-b-estradiol on IK. These results suggested 17-b-estradiol might modulate area postrema neuronal activity by increasing MaxiK current.