The purpose of this study was to determine the effects of 17-β-estradiol on area postrema neuronal activity in vivo and on area postrema potassium currents (IK) in vitro. In anesthetized rats, intravenous injection of 17-β-estradiol (10 ng/kg bw) -inhibited area postrema neuronal activity in 8/8 neurons tested. The averaged firing rate decreased from 2.9 ± 1.1 to 1.1 ± 0.3 Hz. The inhibitory effects of 17-β-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-β-estradiol were examined in dissociated area postrema neurons. In these cells, 17-β-estradiol (0.5 nM) increased the averaged peak IK 27 ± 8%. The time course for the potentiation was observed within ~0.5-1 min after the application of 17-β-estradiol. Full recovery from the potentiation usually occurred within ~3-4 min after the washout of 17-β-estradiol. The biologically inactive 17-α-estradiol had no effect on area postrema IK and the 17-β-estradiol antagonist, ICI 182,780 blocked the effects of 17-β-estradiol on area postrema IK. Finally, big conductance calcium-activated potassium current (MaxiK+) was identified in area postrema neurons (n = 12/12). Blockade of MaxiK+ with 100 nM iberiotoxin blocked the effects of 17-β-estradiol on IK. These results suggested 17-β-estradiol might modulate area postrema neuronal activity by increasing MaxiK+ current.
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