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- W2140906019 abstract "Estrogens act within the ventromedial nucleus of the hypothalamus (VMN) to facilitate lordosis behavior. Estradiol treatment in vivo induces α 1b -adrenoreceptor mRNA and increases the density of α 1B -adrenoreceptor binding in the hypothalamus. Activation of hypothalamic α 1 -adrenoceptors also facilitates estrogen-dependent lordosis. To investigate the cellular mechanisms of adrenergic effects on VMN neurons, whole-cell patch-clamp recordings were carried out on hypothalamic slices from control and estradiol-treated female rats. In control slices, bath application of the α 1 -agonist phenylephrine (PHE; 10 μM) depolarized 10 of 25 neurons (40%), hyperpolarized three neurons (12%), and had no effect on 12 neurons (48%). The depolarization was associated with decreased membrane conductance, and this current had a reversal potential close to the K + equilibrium potential. The α 1b -receptor antagonist chloroethylclonidine (10 μM) blocked the depolarization produced by PHE in all cells. From estradiol-treated rats, significantly more neurons in slices depolarized (71%) and fewer neurons showed no response (17%) to PHE. PHE-induced depolarizations were significantly attenuated with 4-aminopyridine (5 mM) but unaffected by tetraethylammonium chloride (20 mM) or blockers of Na + and Ca 2+ channels. These data indicate that α 1 -adrenoceptors depolarize VMN neurons by reducing membrane conductance for K + . Estradiol amplifies α 1b -adrenergic signaling by increasing the proportion of VMN neurons that respond to stimulation of α 1b -adrenergic receptors, which is expected in turn to promote lordosis." @default.
- W2140906019 created "2016-06-24" @default.
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- W2140906019 date "2008-05-20" @default.
- W2140906019 modified "2023-09-27" @default.
- W2140906019 title "Estradiol modulation of phenylephrine-induced excitatory responses in ventromedial hypothalamic neurons of female rats" @default.
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- W2140906019 doi "https://doi.org/10.1073/pnas.0802760105" @default.
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