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The Journal of Neurophysiology Vol. 84 No. 3 September 2000, pp. 1385-1391
Copyright ©2000 by the American Physiological Society
-Estradiol Modulation of Area Postrema Potassium Currents
Dalton Cardiovascular Research Center, Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211
Li, Zhicheng and
Meredith Hay.
17-
-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-
-estradiol on area postrema neuronal activity in vivo and on area
postrema potassium currents (IK) in vitro. In anesthetized rats,
intravenous injection of 17-
-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-
-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-
-estradiol were examined in dissociated area postrema neurons. In these cells, 17-
-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-
-estradiol. Full recovery from the potentiation usually occurred within ~3-4 min after the washout of 17-
-estradiol. The biologically inactive 17-
-estradiol had no effect on area postrema IK and the
17-
-estradiol antagonist, ICI 182,780 blocked the effects of
17-
-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-
-estradiol on IK. These results suggested 17-
-estradiol might
modulate area postrema neuronal activity by increasing
MaxiK+ current.
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